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The association between schizophrenia and decreased vitamin D levels is well documented. Low maternal and postnatal vitamin D levels suggest a possible etiological mechanism. Alternatively, vitamin D deficiency in patients with schizophrenia is presumably (also) the result of disease-related factors or demographic risk factors such as urbanicity.
In a study population of 347 patients with psychotic disorder and 282 controls, group differences in vitamin D concentration were examined. Within the patient group, associations between vitamin D, symptom levels and clinical variables were analyzed. Group × urbanicity interactions in the model of vitamin D concentration were examined. Both current urbanicity and urbanicity at birth were assessed.
Vitamin D concentrations were significantly lower in patients (B = −8.05; 95% confidence interval (CI) −13.68 to −2.42; p = 0.005). In patients, higher vitamin D concentration was associated with lower positive (B = −0.02; 95% CI −0.04 to 0.00; p = 0.049) and negative symptom levels (B = −0.03; 95% CI −0.05 to −0.01; p = 0.008). Group differences were moderated by urbanicity at birth (χ2 = 6.76 and p = 0.001), but not by current urbanicity (χ2 = 1.50 and p = 0.224). Urbanicity at birth was negatively associated with vitamin D concentration in patients (B = −5.11; 95% CI −9.41 to −0.81; p = 0.020), but not in controls (B = 0.72; 95% CI −4.02 to 5.46; p = 0.765).
Lower vitamin D levels in patients with psychotic disorder may in part reflect the effect of psychosis risk mediated by early environmental adversity. The data also suggest that lower vitamin D and psychopathology may be related through direct or indirect mechanisms.
Identifying factors that influence the functional outcome is an important goal in schizophrenia research. The 22q11.2 deletion syndrome (22q11DS) is a unique genetic model with high risk (20–25%) for schizophrenia. This study aimed to identify potentially targetable domains of neurocognitive functioning associated with functional outcome in adults with 22q11DS.
We used comprehensive neurocognitive test data available for 99 adults with 22q11DS (n = 43 with schizophrenia) and principal component analysis to derive four domains of neurocognition (Verbal Memory, Visual and Logical Memory, Motor Performance, and Executive Performance). We then investigated the association of these neurocognitive domains with adaptive functioning using Vineland Adaptive Behavior Scales data and a linear regression model that accounted for the effects of schizophrenia status and overall intellectual level.
The regression model explained 46.8% of the variance in functional outcome (p < 0.0001). Executive Performance was significantly associated with functional outcome (p = 0.048). Age and schizophrenia were also significant factors. The effects of Executive Performance on functioning did not significantly differ between those with and without psychotic illness.
The findings provide the impetus for further studies to examine the potential of directed (early) interventions targeting Executive Performance to improve long-term adaptive functional outcome in individuals with, or at high risk for, schizophrenia. Moreover, the neurocognitive test profiles may benefit caregivers and clinicians by providing insight into the relative strengths and weaknesses of individuals with 22q11DS, with and without psychotic illness.
A range of endophenotypes characterise psychosis, however there has been limited work understanding if and how they are inter-related.
This multi-centre study includes 8754 participants: 2212 people with a psychotic disorder, 1487 unaffected relatives of probands, and 5055 healthy controls. We investigated cognition [digit span (N = 3127), block design (N = 5491), and the Rey Auditory Verbal Learning Test (N = 3543)], electrophysiology [P300 amplitude and latency (N = 1102)], and neuroanatomy [lateral ventricular volume (N = 1721)]. We used linear regression to assess the interrelationships between endophenotypes.
The P300 amplitude and latency were not associated (regression coef. −0.06, 95% CI −0.12 to 0.01, p = 0.060), and P300 amplitude was positively associated with block design (coef. 0.19, 95% CI 0.10–0.28, p < 0.001). There was no evidence of associations between lateral ventricular volume and the other measures (all p > 0.38). All the cognitive endophenotypes were associated with each other in the expected directions (all p < 0.001). Lastly, the relationships between pairs of endophenotypes were consistent in all three participant groups, differing for some of the cognitive pairings only in the strengths of the relationships.
The P300 amplitude and latency are independent endophenotypes; the former indexing spatial visualisation and working memory, and the latter is hypothesised to index basic processing speed. Individuals with psychotic illnesses, their unaffected relatives, and healthy controls all show similar patterns of associations between endophenotypes, endorsing the theory of a continuum of psychosis liability across the population.
Malaria elimination is on global agendas following successful transmission reductions. Nevertheless moving from low to zero transmission is challenging. South Africa has an elimination target of 2018, which may or may not be realised in its hypoendemic areas.
The Agincourt Health and Demographic Surveillance System has monitored population health in north-eastern South Africa since 1992. Malaria deaths were analysed against individual factors, socioeconomic status, labour migration and weather over a 21-year period, eliciting trends over time and associations with covariates.
Of 13 251 registered deaths over 1.58 million person-years, 1.2% were attributed to malaria. Malaria mortality rates increased from 1992 to 2013, while mean daily maximum temperature rose by 1.5 °C. Travel to endemic Mozambique became easier, and malaria mortality increased in higher socioeconomic groups. Overall, malaria mortality was significantly associated with age, socioeconomic status, labour migration and employment, yearly rainfall and higher rainfall/temperature shortly before death.
Malaria persists as a small but important cause of death in this semi-rural South African population. Detailed longitudinal population data were crucial for these analyses. The findings highlight practical political, socioeconomic and environmental difficulties that may also be encountered elsewhere in moving from low-transmission scenarios to malaria elimination.
Our understanding of the complex relationship between schizophrenia symptomatology and etiological factors can be improved by studying brain-based correlates of schizophrenia. Research showed that impairments in value processing and executive functioning, which have been associated with prefrontal brain areas [particularly the medial orbitofrontal cortex (MOFC)], are linked to negative symptoms. Here we tested the hypothesis that MOFC thickness is associated with negative symptom severity.
This study included 1985 individuals with schizophrenia from 17 research groups around the world contributing to the ENIGMA Schizophrenia Working Group. Cortical thickness values were obtained from T1-weighted structural brain scans using FreeSurfer. A meta-analysis across sites was conducted over effect sizes from a model predicting cortical thickness by negative symptom score (harmonized Scale for the Assessment of Negative Symptoms or Positive and Negative Syndrome Scale scores).
Meta-analytical results showed that left, but not right, MOFC thickness was significantly associated with negative symptom severity (βstd = −0.075; p = 0.019) after accounting for age, gender, and site. This effect remained significant (p = 0.036) in a model including overall illness severity. Covarying for duration of illness, age of onset, antipsychotic medication or handedness weakened the association of negative symptoms with left MOFC thickness. As part of a secondary analysis including 10 other prefrontal regions further associations in the left lateral orbitofrontal gyrus and pars opercularis emerged.
Using an unusually large cohort and a meta-analytical approach, our findings point towards a link between prefrontal thinning and negative symptom severity in schizophrenia. This finding provides further insight into the relationship between structural brain abnormalities and negative symptoms in schizophrenia.
Public health interest in norovirus (NoV) has increased in recent years following improved diagnostics, global burden estimates and the development of NoV vaccine candidates. This study aimed to describe the detection rate, clinical characteristics and environmental features associated with NoV detection in hospitalized children <5 years with diarrhoea in South Africa (SA). Between 2009 and 2013, prospective diarrhoeal surveillance was conducted at four sites in SA. Stool specimens were collected and screened for NoVs and other enteric pathogens using molecular and serological assays. Epidemiological and clinical data were compared in patients with or without detection of NoV. The study detected NoV in 15% (452/3103) of hospitalized children <5 years with diarrhoea with the majority of disease in children <2 years (92%; 417/452). NoV-positive children were more likely to present with diarrhoea and vomiting (odds ratio (OR) 1·3; 95% confidence interval (CI) 1·1–1·7; P = 0·011) with none-to-mild dehydration (adjusted OR 0·5; 95% CI 0·3–0·7) compared with NoV-negative children. Amongst children testing NoV positive, HIV-infected children were more likely to have prolonged hospitalization and increased mortality compared with HIV-uninfected children. Continued surveillance will be important to consider the epidemic trends and estimate the burden and risk of NoV infection in SA.
Many studies have shown associations between a history of childhood trauma and more severe or complex clinical features of bipolar disorders (BD), including suicide attempts and earlier illness onset. However, the psychopathological mechanisms underlying these associations are still unknown. Here, we investigated whether affective lability mediates the relationship between childhood trauma and the severe clinical features of BD.
A total of 342 participants with BD were recruited from France and Norway. Diagnosis and clinical characteristics were assessed using the Diagnostic Interview for Genetic Studies (DIGS) or the Structured Clinical Interview for DSM-IV Axis I disorders (SCID-I). Affective lability was measured using the short form of the Affective Lability Scale (ALS-SF). A history of childhood trauma was assessed using the Childhood Trauma Questionnaire (CTQ). Mediation analyses were performed using the SPSS process macro.
Using the mediation model and covariation for the lifetime number of major mood episodes, affective lability was found to statistically mediate the relationship between childhood trauma experiences and several clinical variables, including suicide attempts, mixed episodes and anxiety disorders. No significant mediation effects were found for rapid cycling or age at onset.
Our data suggest that affective lability may represent a psychological dimension that mediates the association between childhood traumatic experiences and the risk of a more severe or complex clinical expression of BD.
Africa is experiencing a rapid increase in adult obesity and associated cardiometabolic diseases (CMDs). The H3Africa AWI-Gen Collaborative Centre was established to examine genomic and environmental factors that influence body composition, body fat distribution and CMD risk, with the aim to provide insights towards effective treatment and intervention strategies. It provides a research platform of over 10 500 participants, 40–60 years old, from Burkina Faso, Ghana, Kenya and South Africa. Following a process that involved community engagement, training of project staff and participant informed consent, participants were administered detailed questionnaires, anthropometric measurements were taken and biospecimens collected. This generated a wealth of demographic, health history, environmental, behavioural and biomarker data. The H3Africa SNP array will be used for genome-wide association studies. AWI-Gen is building capacity to perform large epidemiological, genomic and epigenomic studies across several African counties and strives to become a valuable resource for research collaborations in Africa.
Poor educational achievement is associated with a range of psychiatric disorders. Several studies suggest that this underperformance is due to cognitive deficits that commence before disease onset and reflect a genetic risk for this disorder. However, the specificity and the familial contribution of this cognitive deficit are not clear. We analysed lifetime educational achievement of psychiatric patients diagnosed with schizophrenia, bipolar or depressive disorder and their unaffected siblings.
In a register-based case-control study, 1561 patients with schizophrenia, 813 patients with bipolar disorder, 8112 patients with depression, and their siblings were each matched with eight population controls. Patients, siblings and controls were compared on the highest educational stream they completed.
Lower educational achievement was present in schizophrenia patients from primary school onwards [completing primary school: odds ratio (OR) 0.69; completing secondary school: OR 0.69; completing academic education: OR 0.46], compared to patients with bipolar disorder or depression. Siblings of schizophrenia, bipolar or depressed patients showed no underachievement at primary or secondary school, but siblings of schizophrenia patients as well as siblings of depressed patients were less successful in their educational achievement after secondary school (completing academic education, schizophrenia siblings: OR 0.90; depressive disorder siblings: OR 0.91).
Educational underachievement from primary school onwards is specifically related to schizophrenia and not to bipolar disorder or depression. Moreover, it appears to be a harbinger of the illness, since it is not found in their siblings. These results add to evidence that early cognitive deficits are a distinct feature of the schizophrenia phenotype.
The purpose of this qualitative evaluation was to explore the experience of implementing routine telemonitoring (TM) in real-world primary care settings from the perspective of those delivering the intervention; namely the TM staff, and report on lessons learned that could inform future projects of this type.
Routine TM for high-risk patients within primary care practices may help improve chronic disease control and reduce complications, including unnecessary hospital admissions. However, little is known about how to integrate routine TM in busy primary care practices. A TM pilot for diabetic patients was attempted in six primary care practices as part of the Beacon Community in Western New York.
Semi-structured interviews were conducted with representatives of three TM agencies (n=8) participating in the pilot. Interviews were conducted over the phone or in person and lasted ~30 min. Interviews were audio-taped and transcribed. Analysis was conducted using immersion-crystallization to identify themes.
TM staff revealed several themes related to the experience of delivering TM in real-world primary care: (1) the nurse–patient relationship is central to a successful TM experience, (2) TM is a useful tool for understanding socio-economic context and its impact on patients’ health, (3) TM staff anecdotally report important potential impacts on patient health, and (4) integrating TM into primary care practices needs to be planned carefully.
This qualitative study identified challenges and unexpected benefits that might inform future efforts. Communication and integration between the TM agency and the practice, including the designation of a point person within the office to coordinate TM and help address the broader contextual needs of patients, are important considerations for future implementation. The role of the TM nurse in developing trust with patients and uncovering the social and economic context within which patients manage their diabetes was an unexpected benefit.
Although additional surveys with large Schmidt telescopes continue to yield small catches of additional planetaries (Kohoutek) one cannot escape the conclusion that most planetaries available to existing equipment have been detected. Much remains to be done with powerful Schmidt equipment in the southern hemisphere, especially in the Magellanic Clouds. A vast body of photometric and spectroscopic observation needs to be garnered for the numerous faint nebulae so far discovered.
Spectroscopic and spectrophotometric studies have been carried out for most bright planetaries (λ < 5800) but much remains to be done in the red and near infrared. Important advances have been made in the far infrared (~10μ) (Gillett, Low, Stein, Woolf) where a number of planetaries seem to show abnormally strong continua. This abnormally intense radiation has been attributed to non-thermal emission, effects of many faint lines, and to thermal emission by dust grains (Krishna Swamy, O’Dell) with perhaps the bulk of the evidence favoring the last-mentioned hypothesis. An increasing number of radio observations from 9·5 mm to 73 cm (Thompson, Colvin, Stanley, LeMarne, Kaftan-Kassim, Babieri and Ficarra, Terzian, L. Aller and Milne, Hughes) all indicate that planetaries are thermal sources.
We present Chandra HETG spectra of seven cataclysmic variables, including four intermediate polars. We find that they divide unambiguously into two distinct types. Spectra of the first type (nonmagnetic systems and EX Hya) are remarkably well fit by a simple cooling flow model, which assumes only steady-state isobaric radiative cooling. The maximum temperature, kTmax, and the normalization, which provides a highly precise measurement of the accretion rate, are the only free parameters of this model. Spectra of the second type (the three other IPs) are grossly inconsistent with a cooling flow model. They instead exhibit a hard continuum, and show strong H-like and He-like ion emission but little Fe L-shell emission, which is consistent with expectations for line emission from a photoionized plasma. Using a simple photoionization model, we argue that the observed line emission for these sources can be driven entirely by the hard continuum. The physical significance of these two distinct types of X-ray spectra is also explored.
A multi-faceted, multi-institutional laboratory astrophysics program is carried out at the Livermore electron beam ion trap facility, which is a mature spectroscopic source with unsurpassed controls and capabilities, and an unparalleled assortment of spectroscopic equipment, including a full complement of grating and crystal spectrometers and a 6x6 micro-calorimeter array. Recent results range from the calibration of x-ray diagnostics, including the Fe XVII and Fe XXV emission lines, extensive lists of L-shell ions, the first laboratory simulation and fit of a cometary x-ray emission spectrum, and the discovery of new spectral diagnostics for measuring magnetic field strengths.
The contribution of subsidized food commodities to total food consumption is unknown. We estimated the proportion of individual energy intake from food commodities receiving the largest subsidies from 1995 to 2010 (corn, soyabeans, wheat, rice, sorghum, dairy and livestock).
Integrating information from three federal databases (MyPyramid Equivalents, Food Intakes Converted to Retail Commodities, and What We Eat in America) with data from the 2001–2006 National Health and Nutrition Examination Surveys, we computed a Subsidy Score representing the percentage of total energy intake from subsidized commodities. We examined the score’s distribution and the probability of having a ‘high’ (≥70th percentile) v. ‘low’ (≤30th percentile) score, across the population and subgroups, using multivariate logistic regression.
Community-dwelling adults in the USA.
Participants (n 11 811) aged 18–64 years.
Median Subsidy Score was 56·7 % (interquartile range 47·2–65·4 %). Younger, less educated, poorer, and Mexican Americans had higher scores. After controlling for covariates, age, education and income remained independently associated with the score: compared with individuals aged 55–64 years, individuals aged 18–24 years had a 50 % higher probability of having a high score (P<0·0001). Individuals reporting less than high-school education had 21 % higher probability of having a high score than individuals reporting college completion or higher (P=0·003); individuals in the lowest tertile of income had an 11 % higher probability of having a high score compared with individuals in the highest tertile (P=0·02).
Over 50 % of energy in US diets is derived from federally subsidized commodities.
Smaller hippocampal volume has often been observed in patients with post-traumatic stress disorder (PTSD). However, there is no consensus whether this is a result of stress/trauma exposure, or constitutes a vulnerability factor for the development of PTSD. Second, it is unclear whether hippocampal volume normalizes with successful treatment of PTSD, or whether a smaller hippocampus is a risk factor for the persistence of PTSD.
Magnetic resonance imaging (MRI) scans and clinical interviews were collected from 47 war veterans with PTSD, 25 healthy war veterans (combat controls) and 25 healthy non-military controls. All veterans were scanned a second time with a 6- to 8-month interval, during which PTSD patients received trauma-focused therapy. Based on post-treatment PTSD symptoms, patients were divided into a PTSD group who was in remission (n = 22) and a group in whom PTSD symptoms persisted (n = 22). MRI data were analysed with Freesurfer.
Smaller left hippocampal volume was observed in PTSD patients compared with both control groups. Hippocampal volume of the combat controls did not differ from healthy controls. Second, pre- and post-treatment analyses of the PTSD patients and combat controls revealed reduced (left) hippocampal volume only in the persistent patients at both time points. Importantly, hippocampal volume did not change with treatment.
Our findings suggest that a smaller (left) hippocampus is not the result of stress/trauma exposure. Furthermore, hippocampal volume does not increase with successful treatment. Instead, we demonstrate for the first time that a smaller (left) hippocampus constitutes a risk factor for the persistence of PTSD.
Glass sponge reefs on the continental shelf of western Canada and south-east Alaska are considered stable deep-sea habitats that do not change significantly over time. Research cruises using a remotely operated vehicle equipped with accurate GPS positioning have allowed us to observe the same sponges at two reefs in the Strait of Georgia, British Columbia to document recruitment, growth and response to damage over time. Spermatocysts and putative embryos found in winter suggest annual, asynchronous reproduction. Juvenile sponges (2–10 cm in osculum diameter) in densities up to 1 m−2 were more concentrated near live sponges and sponge skeletons than away (Spearman rank correlations, P < 0.0001 for live cover and for skeletons), suggesting that recruitment occurs in particular regions using sponge skeletons as substrate. Most sponges showed no change in shape or size over 2–3 years, but some had died while others showed growth of 1–9 cm year−1. Deposition rates of reef-cementing sediments were 97 mm year−1 at Galiano Reef and 137 mm year−1 at Fraser Reef, but sediments eroded so that there was no net gain or loss over time. Sponges recovered within 1 year from small-scale damage that mimicked bites by fish or nudibranchs; however sponges did not recover from crushing of a large area (1.5 × 2 m2) even 3 years later. These observations and experiments show that while recruitment and growth of sponge reefs is more dynamic than previously thought, the reefs are not resilient in the face of larger-scale disturbances such as might be inflicted by trawling.
Post-traumatic stress disorder (PTSD) is thought to be characterized by general heightened amygdala activation. However, this hypothesis is mainly based on specific studies presenting fear or trauma-related stimuli, hence, a thorough investigation of trauma-unrelated emotional processing in PTSD is needed.
In this study, 31 male medication-naive veterans with PTSD, 28 male control veterans (combat controls; CC) and 25 non-military men (healthy controls; HC) were included. Participants underwent functional MRI while trauma-unrelated neutral, negative and positive emotional pictures were presented. In addition to the group analyses, PTSD patients with and without major depressive disorder (MDD) were compared.
All groups showed an increased amygdala response to negative and positive contrasts, but amygdala activation did not differ between groups. However, a heightened dorsal anterior cingulate cortex (dACC) response for negative contrasts was observed in PTSD patients compared to HC. The medial superior frontal gyrus was deactivated in the negative contrast in HC, but not in veterans. PTSD+MDD patients showed decreased subgenual ACC (sgACC) activation to all pictures compared to PTSD–MDD.
Our findings do not support the hypothesis that increased amygdala activation in PTSD generalizes to trauma-unrelated emotional processing. Instead, the increased dACC response found in PTSD patients implicates an attentional bias that extends to trauma-unrelated negative stimuli. Only HC showed decreased medial superior frontal gyrus activation. Finally, decreased sgACC activation was related to MDD status within the PTSD group.
The association between childhood trauma and psychotic and depressive symptomatology is well established. However, less is known about the specificity and course of these symptoms in relation to childhood trauma.
In a large sample (n = 2765) of patients with psychosis (n = 1119), their siblings (n = 1057) and controls (n = 589), multivariate (mixed-effects) regression analyses with multiple outcomes were performed to examine the association between childhood trauma and psychotic and depressive symptomatology over a 3-year period.
A dose–response relationship was found between childhood trauma and psychosis. Abuse was more strongly associated with positive symptoms than with negative symptoms whereas the strength of the associations between neglect and positive and negative symptoms was comparable. In patients, similar associations between childhood trauma and psychotic or depressive symptoms were found, and in siblings and controls, stronger associations were found between trauma and depressive symptomatology. Childhood trauma was not related to a differential course of symptoms over a 3-year time period.
In congruence with earlier work, our findings suggest that childhood trauma, and abuse in particular, is associated with (subthreshold) psychosis. However, childhood trauma does not seem to be associated with a differential course of symptoms, nor does it uniquely heighten the chance of developing (subthreshold) psychotic symptomatology. Our results indicate that trauma may instead contribute to a shared vulnerability for psychotic and depressive symptoms.
The risk of developing bipolar disorder (BD) has been linked to structural brain abnormalities. The degree to which genes and environment influence the association of BD with cortical surface area remains to be elucidated. In this twin study, genetic and environmental contributions to the association between liability to develop BD and surface area, thickness and volume of the cortex were examined.
The study cohort included 44 affected monozygotic (nine concordant, 12 discordant) and dizygotic (four concordant, 19 discordant) twin pairs, and seven twins from incomplete discordant monozygotic and dizygotic discordant twin pairs. In addition, 37 monozygotic and 24 dizygotic healthy control twin pairs, and six twins from incomplete monozygotic and dizygotic control pairs were included.
Genetic liability to develop BD was associated with a larger cortical surface in limbic and parietal regions, and a thicker cortex in central and parietal regions. Environmental factors related to BD were associated with larger medial frontal, parietal and limbic, and smaller orbitofrontal surfaces. Furthermore, thinner frontal, limbic and occipital cortex, and larger frontal and parietal, and smaller orbitofrontal volumes were also associated with environmental factors related to BD.
Our results suggest that unique environmental factors play a prominent role in driving the associations between liability to develop BD and cortical measures, particularly those involving cortical thickness. Further evaluation of their influence on the surface and thickness of the cortical mantle is recommended. In addition, cortical volume appeared to be primarily dependent on surface and not thickness.