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A new fossil site in a previously unexplored part of western Madagascar (the Beanka Protected Area) has yielded remains of many recently extinct vertebrates, including giant lemurs (Babakotia radofilai, Palaeopropithecus kelyus, Pachylemur sp., and Archaeolemur edwardsi), carnivores (Cryptoprocta spelea), the aardvark-like Plesiorycteropus sp., and giant ground cuckoos (Coua). Many of these represent considerable range extensions. Extant species that were extirpated from the region (e.g., Prolemur simus) are also present. Calibrated radiocarbon ages for 10 bones from extinct primates span the last three millennia. The largely undisturbed taphonomy of bone deposits supports the interpretation that many specimens fell in from a rock ledge above the entrance. Some primates and other mammals may have been prey items of avian predators, but human predation is also evident. Strontium isotope ratios (87Sr/86Sr) suggest that fossils were local to the area. Pottery sherds and bones of extinct and extant vertebrates with cut and chop marks indicate human activity in previous centuries. Scarcity of charcoal and human artifacts suggests only occasional visitation to the site by humans. The fossil assemblage from this site is unusual in that, while it contains many sloth lemurs, it lacks ratites, hippopotami, and crocodiles typical of nearly all other Holocene subfossil sites on Madagascar.
To achieve their conservation goals individuals, communities and organizations need to acquire a diversity of skills, knowledge and information (i.e. capacity). Despite current efforts to build and maintain appropriate levels of conservation capacity, it has been recognized that there will need to be a significant scaling-up of these activities in sub-Saharan Africa. This is because of the rapid increase in the number and extent of environmental problems in the region. We present a range of socio-economic contexts relevant to four key areas of African conservation capacity building: protected area management, community engagement, effective leadership, and professional e-learning. Under these core themes, 39 specific recommendations are presented. These were derived from multi-stakeholder workshop discussions at an international conference held in Nairobi, Kenya, in 2015. At the meeting 185 delegates (practitioners, scientists, community groups and government agencies) represented 105 organizations from 24 African nations and eight non-African nations. The 39 recommendations constituted six broad types of suggested action: (1) the development of new methods, (2) the provision of capacity building resources (e.g. information or data), (3) the communication of ideas or examples of successful initiatives, (4) the implementation of new research or gap analyses, (5) the establishment of new structures within and between organizations, and (6) the development of new partnerships. A number of cross-cutting issues also emerged from the discussions: the need for a greater sense of urgency in developing capacity building activities; the need to develop novel capacity building methodologies; and the need to move away from one-size-fits-all approaches.
Low birth weight is associated with increased risk of cardiovascular disease in adulthood. Intrauterine growth restriction (IUGR) hearts have fewer CMs in early postnatal life, which may impair postnatal cardiovascular function and hence, explain increased disease risk, but whether the cardiomyocyte deficit persists to adult life is unknown. We therefore studied the effects of experimentally induced placental restriction (PR) on cardiac outcomes in young adult sheep. Heart size, cardiomyocyte number, nuclearity and size were measured in control (n=5) and PR (n=5) male sheep at 1 year of age. PR lambs were 36% lighter at birth (P=0.007), had 38% faster neonatal relative growth rates (P=0.001) and had 21% lighter heart weights relative to body weight as adults (P=0.024) than control lambs. Cardiomyocyte number, nuclearity and size in the left ventricle did not differ between control and PR adults; hearts of both groups contained cardiomyocytes (CM) with between one and four nuclei. Overall, cardiomyocyte number in the adult left ventricle correlated positively with birth weight but not with adult weight. This study is the first to demonstrate that intrauterine growth directly influences the complement of CM in the adult heart. Cardiomyocyte size was not correlated with cardiomyocyte number or birth weight. Our results suggest that body weight at birth affects lifelong cardiac functional reserve. We hypothesise that decreased cardiomyocyte number of low birth weight individuals may impair their capacity to adapt to additional challenges such as obesity and ageing.
Objectives: To examine whether apolipoprotein e4 (APOE) status moderates the association of family environment with child functioning following early traumatic brain injury (TBI). Methods: Sixty-five children with moderate to severe TBI and 70 children with orthopedic injury (OI) completed assessments 6, 12, 18 months, and 3.5 and 6.8 years post injury. DNA was extracted from saliva samples and genotyped for APOE e4 status. Linear mixed models examined moderating effects of APOE e4 status on associations between two family environment factors (parenting style, home environment) and three child outcomes (executive functioning, behavioral adjustment, adaptive functioning). Results: Children with TBI who were carriers of the e4 allele showed poorer adaptive functioning relative to non-carriers with TBI and children with OI in the context of low authoritarianism. At high levels of authoritarianism, non-carriers with TBI showed the poorest adaptive functioning among groups. There were no main effects or interactions involving APOE and executive functioning or behavioral adjustment. Conclusions:The APOE e4 allele was detrimental for long-term adaptive functioning in the context of positive parenting, whereas in less optimal parenting contexts, being a non-carrier was detrimental. We provide preliminary evidence for an interaction of APOE e4 status and parenting style in predicting long-term outcomes following early TBI. (JINS, 2016, 22, 859–864)
Major depressive disorder (MDD) is a common and disabling condition with well-established heritability and environmental risk factors. Gene–environment interaction studies in MDD have typically investigated candidate genes, though the disorder is known to be highly polygenic. This study aims to test for interaction between polygenic risk and stressful life events (SLEs) or childhood trauma (CT) in the aetiology of MDD.
The RADIANT UK sample consists of 1605 MDD cases and 1064 controls with SLE data, and a subset of 240 cases and 272 controls with CT data. Polygenic risk scores (PRS) were constructed using results from a mega-analysis on MDD by the Psychiatric Genomics Consortium. PRS and environmental factors were tested for association with case/control status and for interaction between them.
PRS significantly predicted depression, explaining 1.1% of variance in phenotype (p = 1.9 × 10−6). SLEs and CT were also associated with MDD status (p = 2.19 × 10−4 and p = 5.12 × 10−20, respectively). No interactions were found between PRS and SLEs. Significant PRSxCT interactions were found (p = 0.002), but showed an inverse association with MDD status, as cases who experienced more severe CT tended to have a lower PRS than other cases or controls. This relationship between PRS and CT was not observed in independent replication samples.
CT is a strong risk factor for MDD but may have greater effect in individuals with lower genetic liability for the disorder. Including environmental risk along with genetics is important in studying the aetiology of MDD and PRS provide a useful approach to investigating gene–environment interactions in complex traits.
Nitrous oxide (N2O) emissions associated with urine nitrogen (N) deposition during grazing are a major component of greenhouse gas emissions from domestic livestock. The present study investigated the relationship between urine N loading rate and the efficacy of a nitrification inhibitor, dicyandiamide (DCD), on cumulative N2O emissions from a grassland soil in Ireland over 80 and 360-day periods in 2009/10 and 2010/11. A diminishing curvilinear relationship between urine N rate and cumulative N2O emissions was observed in both years. Despite this increase in cumulative N2O emissions, the emission factor (EF3) for N2O decreased with increasing urine N rate from, on average, 0·24 to 0·10% (urine applied at 300 and 1000 kg N/ha, respectively), during an 80-day measurement period. This was probably the result of a factor other than N, such as carbon (C), limiting the production of N2O. The efficacy of DCD varied with urine N loading rate, and inter-annual variability in efficacy was also observed. Dicyandiamide was effective at reducing N2O production for 50–80 days after urine application, which accounted for the major period of elevated daily flux. However, DCD was ineffective at reducing N2O production after this period, which was likely a result of its removal from the soil via degradation and leaching.
Recent data provide strong support for a substantial common polygenic contribution (i.e. many alleles each of small effect) to genetic susceptibility for schizophrenia and overlapping susceptibility for bipolar disorder.
To test hypotheses about the relationship between schizophrenia and psychotic types of bipolar disorder.
Using a polygenic score analysis to test whether schizophrenia polygenic risk alleles, en masse, significantly discriminate between individuals with bipolar disorder with and without psychotic features. The primary sample included 1829 participants with bipolar disorder and the replication sample comprised 506 people with bipolar disorder.
The subset of participants with Research Diagnostic Criteria schizoaffective bipolar disorder (n = 277) were significantly discriminated from the remaining participants with bipolar disorder (n = 1552) in both the primary (P = 0.00059) and the replication data-sets (P = 0.0070). In contrast, those with psychotic bipolar disorder as a whole were not significantly different from those with non-psychotic bipolar disorder in either data-set.
Genetic susceptibility influences at least two major domains of psychopathological variation in the schizophrenia–bipolar disorder clinical spectrum: one that relates to expression of a ‘bipolar disorder-like’ phenotype and one that is associated with expression of ‘schizophrenia-like’ psychotic symptoms.
In the UK, South Asian adults have increased risks of CHD, type 2 diabetes and central obesity. Black African-Caribbeans, in contrast, have increased risks of type 2 diabetes and general obesity but lower CHD risk. There is growing evidence that these risk differences emerge in early life and that nutritional factors may be important. We have therefore examined the variations in nutritional composition of the diets of South Asian, black African-Caribbean and white European children, using 24 h recalls of dietary intake collected during a cross-sectional survey of cardiovascular health in eighty-five primary schools in London, Birmingham and Leicester. In all, 2209 children aged 9–10 years took part, including 558 of South Asian, 560 of black African-Caribbean and 543 of white European ethnicity. Compared with white Europeans, South Asian children reported higher mean total energy intake; their intakes of total fat, polyunsaturated fat and protein (both absolute and as proportions of total energy intake) were higher and their intakes of carbohydrate as a proportion of energy (particularly sugars), vitamin C and D, Ca and haem Fe were lower. These differences were especially marked for Bangladeshi children. Black African-Caribbean children had lower intakes of total and saturated fat (both absolute and as proportions of energy intake), NSP, vitamin D and Ca. The lower total and saturated fat intakes were particularly marked among black African children. Appreciable ethnic differences exist in the nutritional composition of children's diets, which may contribute to future differences in chronic disease risk.
This brief report describes the first year of a joint Cambridge University—Iceland University two-year project to develop radio echo depth-sounding apparatus suitable for the temperate ice of the Vatnajökull ice cap. There is much interest in obtaining detailed ice thickness measurements for the 8 400 km2 Vatnajökull area, where only limited ice-depth surveys, using bore-hole and seismxic techniques, have been carried out in the past. A line of volcanic and geothermal activity extends through the western regions of the ice and creates a sub-glacial lake, Grimsvotn, which collapses every five years or so giving rise to the jökulhlaups, a catastrophic flooding which affects considerable areas of the Icelandic coast to the south of Vatnajökull. Proper understanding of the jökulhlaups phenomena can only be achieved if detailed knowledge of ice thickness and related data are available. Established radio echo sounding techniques which have been successfully applied in the polar regions do not work in water-laden ice such as is to be found in the Vatnajökull area.
Psychiatric phenotypes are currently defined according to sets of
descriptive criteria. Although many of these phenotypes are heritable, it
would be useful to know whether any of the various diagnostic categories
in current use identify cases that are particularly helpful for
To use genome-wide genetic association data to explore the relative
genetic utility of seven different descriptive operational diagnostic
categories relevant to bipolar illness within a large UK case–control
bipolar disorder sample.
We analysed our previously published Wellcome Trust Case Control
Consortium (WTCCC) bipolar disorder genome-wide association data-set,
comprising 1868 individuals with bipolar disorder and 2938 controls
genotyped for 276 122 single nucleotide polymorphisms (SNPs) that met
stringent criteria for genotype quality. For each SNP we performed a test
of association (bipolar disorder group v. control group) and used the
number of associated independent SNPs statistically significant at
P<0.00001 as a metric for the overall genetic
signal in the sample. We next compared this metric with that obtained
using each of seven diagnostic subsets of the group with bipolar
disorder: Research Diagnostic Criteria (RDC): bipolar I disorder; manic
disorder; bipolar II disorder; schizoaffective disorder, bipolar type;
DSM–IV: bipolar I disorder; bipolar II disorder; schizoaffective
disorder, bipolar type.
The RDC schizoaffective disorder, bipolar type (v.
controls) stood out from the other diagnostic subsets as having a
significant excess of independent association signals
(P<0.003) compared with that expected in samples of
the same size selected randomly from the total bipolar disorder group
data-set. The strongest association in this subset of participants with
bipolar disorder was at rs4818065 (P = 2.42 ×
10–7). Biological systems implicated included gamma
amniobutyric acid (GABA)A receptors. Genes having at least one
associated polymorphism at P<10–4 included
B3GALTS, A2BP1, GABRB1, AUTS2, BSN, PTPRG, GIRK2 and
Our findings show that individuals with broadly defined bipolar
schizoaffective features have either a particularly strong genetic
contribution or that, as a group, are genetically more homogeneous than
the other phenotypes tested. The results point to the importance of using
diagnostic approaches that recognise this group of individuals. Our
approach can be applied to similar data-sets for other psychiatric and
In a factory population the occurrence of reactions to tetanus toxoid was recorded after 6740 injections. The incidence of general reactions was 0·3 % and of local reactions 2·6%. The local reaction rate to the first injection of the basic immunization course was 0·9%, to the second injection 2·7%, and to the third injection 7·4%. To booster injections the rate was 1·6%. The local reaction rate was appreciably higher in women than in men – 14·4 % and 5·7 % respectively in the case of the third injection – and the incidence among women increased with age.
Tetanus vaccine containing 10 Lf of toxoid caused fewer reactions than one containing 20 Lf, but a reduction in the content of aluminium adjuvant did not affect the reaction rate.
Almost all reactors were found to have a satisfactory serum antitoxin concentration at the time of the reaction or developed a satisfactory immunity within 1–6 months.
Skin tests were made in 32 hypersensitive patients. Neither the diluent, thiomersal preservative, nor the culture medium appeared to be responsible for hypersensitivity. The degree of hypersensitivity elicited by a special highly purified toxoid was only very slightly less than that elicited by the commercially pure toxoid. It is suggested that reactions are largely due to the toxoid antigen itself rather than to impurities or other components of the vaccine.
Functional brain abnormalities have been repeatedly demonstrated in schizophrenia but there is little data concerning their progression. For such studies to have credibility it is first important to establish the reproducibility of functional imaging techniques. The current study aimed to examine these factors in healthy controls and in unmedicated subjects at high genetic risk of the disorder: (i) to examine the reproducibility of task-related activation patterns, (ii) to determine if there were any progressive functional changes in high-risk subjects versus controls reflecting inheritance of the schizophrenic trait, and (iii) to examine changes over time in relation to fluctuating positive psychotic symptoms (i.e. state effects).
Subjects were scanned performing the Hayling sentence completion test on two occasions 18 months apart. Changes in activation were examined in controls and high-risk subjects (n=16, n=63). Reproducibility was assessed for controls and high-risk subjects who remained asymptomatic at both time points (n=16, n=32).
Intra-class correlation values indicated good agreement between scanning sessions. No significant differences over time were seen between the high-risk and control group; however, comparison of high-risk subjects who developed symptoms versus those who remained asymptomatic revealed activation increases in the left middle temporal gyrus (p=0.026).
The current results suggest that functional changes over time occur in the lateral temporal cortex as high genetic risk subjects become symptomatic, further, they indicate the usefulness of functional imaging tools for investigating progressive changes associated with state and trait effects in schizophrenia.
Velo-cardio-facial syndrome (VCFS) is associated with deletions at chromosome 22q11, abnormalities in brain anatomy and function, and schizophrenia-like psychosis. Thus it is assumed that one or more genes within the deleted region are crucial to brain development. However, relatively little is known about how genetic variation at 22q11 affects brain structure and function. One gene on 22q11 is catechol-O-methyltransferase (COMT): an enzyme that degrades dopamine and contains a functional polymorphism (Val158Met) affecting enzyme activity. Here, we investigated the effect of COMT Val158Met polymorphism on brain anatomy and cognition in adults with VCFS.
The COMT Val158Met polymorphism was genotyped for 26 adults with VCFS on whom DNA was available. We explored its effects on regional brain volumes using hand tracing approaches; on regional grey- and white-matter density using computerized voxel-based analyses; and measures of attention, IQ, memory, executive and visuospatial function using a comprehensive neuropsychological test battery.
After corrections for multiple comparisons Val-hemizygous subjects, compared with Met-hemizygotes, had a significantly larger volume of frontal lobes. Also, Val-hemizygotes had significantly increased grey matter density in cerebellum, brainstem, and parahippocampal gyrus, and decreased white matter density in the cerebellum. No significant effects of COMT genotype on neurocognitive performance were found.
COMT genotype effects on brain anatomy in VCFS are not limited to frontal regions but also involve other structures previously implicated in VCFS. This suggests variation in COMT activity is implicated in brain development in VCFS.