Ongoing over-exploitation and delayed responses to environmental change highlight the urgency for action to promote vertebrate recoveries by 2030

To safeguard nature, we must understand the drivers of biodiversity loss. Time-delayed biodiversity responses to environmental changes (ecological lags) are often absent from models of biodiversity change, despite their well-documented existence. We quantify how lagged responses to climate and land-use change have influenced mammal and bird populations around the world, while incorporating effects of direct exploitation and conservation interventions. Ecological lag duration varies between drivers, vertebrate classes and body size groupings-e.g. lags linked to climate-change impacts are 13 years for small birds, rising to 40 years for larger species. Past warming and land conversion generally combine to predict population declines; however, such conditions are associated with population increases for small mammals. Positive effects of management (>+4% annually for large mammals) and protected areas (>+6% annually for large birds) on population trends contrast with the negative impact of exploitation (<-7% annually for birds), highlighting the need to promote sustainable use. Model projections suggest a future with winners (e.g. large birds) and losers (e.g. medium-sized birds), with current/recent environmental change substantially influencing abundance trends to 2050. Without urgent action, including effective conservation interventions and promoting sustainable use, ambitious targets to stop declines by 2030 may already be slipping out of reach

Impact of CONSORT extension for cluster randomised trials on quality of reporting and study methodology : review of random sample of 300 trials, 2000-8

Peer reviewedPublisher PD

Linear optical properties of one-dimensional Frenkel exciton systems with intersite energy correlations

We analyze the effects of intersite energy correlations on the linear optical properties of one-dimensional disordered Frenkel exciton systems. The absorption line width and the factor of radiative rate enhancement are studied as a function of the correlation length of the disorder. The absorption line width monotonously approaches the seeding degree of disorder on increasing the correlation length. On the contrary, the factor of radiative rate enhancement shows a non-monotonous trend, indicating a complicated scenario of the exciton localization in correlated systems. The concept of coherently bound molecules is exploited to explain the numerical results, showing good agreement with theory. Some recent experiments are discussed in the light of the present theory.Comment: 18 pages, 3 figues, REVTeX, to appear in Physical Review

Ongoing over-exploitation and delayed responses to environmental change highlight the urgency for action to promote vertebrate recoveries by 2030

To safeguard nature, we must understand the drivers of biodiversity loss. Time-delayed biodiversity responses to environmental changes (ecological lags) are often absent from models of biodiversity change, despite their well-documented existence. We quantify how lagged responses to climate and land-use change have influenced mammal and bird populations around the world, while incorporating effects of direct exploitation and conservation interventions. Ecological lag duration varies between drivers, vertebrate classes and body size groupings—e.g. lags linked to climate-change impacts are 13 years for small birds, rising to 40 years for larger species. Past warming and land conversion generally combine to predict population declines; however, such conditions are associated with population increases for small mammals. Positive effects of management (>+4% annually for large mammals) and protected areas (>+6% annually for large birds) on population trends contrast with the negative impact of exploitation (<−7% annually for birds), highlighting the need to promote sustainable use. Model projections suggest a future with winners (e.g. large birds) and losers (e.g. medium-sized birds), with current/recent environmental change substantially influencing abundance trends to 2050. Without urgent action, including effective conservation interventions and promoting sustainable use, ambitious targets to stop declines by 2030 may already be slipping out of reach

Examining the Impact of Imputation Errors on Fine-Mapping Using DNA Methylation QTL as a Model Trait

Genetic variants disrupting DNA methylation at CpG dinucleotides (CpG-SNP) provide a set of known causal variants to serve as models for testing fine-mapping methodology. We use 1716 CpG-SNPs to test three fine-mapping approaches (BIMBAM, BSLMM, and the J-test), assessing the impact of imputation errors and the choice of reference panel by using both whole-genome sequence (WGS), and genotype array data on the same individuals (n=1166). The choice of imputation reference panel had a strong effect on imputation accuracy, with the 1000 Genomes Phase 3 (1000G) reference panel (n=2504 from 26 populations) giving a mean non-reference discordance rate between imputed and sequenced genotypes of 3.2% compared to 1.6% when using the Haplotype Reference Consortium (HRC) reference panel (n=32470 Europeans). These imputation errors impacted on whether the CpG-SNP was included in the 95% credible set, with a difference of ∼ 23% and ∼ 7% between the WGS and the 1000G and HRC imputed datasets respectively. All of the fine-mapping methods failed to reach the expected 95% coverage of the CpG-SNP. This is attributed to secondary cis genetic effects that are unable to be statistically separated from the CpG-SNP, and through a masking mechanism where the effect of the methylation disrupting allele at the CpG-SNP is hidden by the effect of a nearby SNP that has strong LD with the CpG-SNP. The reduced accuracy in fine-mapping a known causal variant in a low level biological trait with imputed genetic data has implications for the study of higher order complex traits and disease

Inflammation-driven bone formation in a mouse model of ankylosing spondylitis: sequential not parallel processes

Background\ud \ud Ankylosing spondylitis (AS) is an immune-mediated arthritis particularly targeting the spine and pelvis and is characterised by inflammation, osteoproliferation and frequently ankylosis. Current treatments that predominately target inflammatory pathways have disappointing efficacy in slowing disease progression. Thus, a better understanding of the causal association and pathological progression from inflammation to bone formation, particularly whether inflammation directly initiates osteoproliferation, is required.\ud \ud Methods\ud \ud The proteoglycan-induced spondylitis (PGISp) mouse model of AS was used to histopathologically map the progressive axial disease events, assess molecular changes during disease progression and define disease progression using unbiased clustering of semi-quantitative histology. PGISp mice were followed over a 24-week time course. Spinal disease was assessed using a novel semi-quantitative histological scoring system that independently evaluated the breadth of pathological features associated with PGISp axial disease, including inflammation, joint destruction and excessive tissue formation (osteoproliferation). Matrix components were identified using immunohistochemistry.\ud \ud Results\ud \ud Disease initiated with inflammation at the periphery of the intervertebral disc (IVD) adjacent to the longitudinal ligament, reminiscent of enthesitis, and was associated with upregulated tumor necrosis factor and metalloproteinases. After a lag phase, established inflammation was temporospatially associated with destruction of IVDs, cartilage and bone. At later time points, advanced disease was characterised by substantially reduced inflammation, excessive tissue formation and ectopic chondrocyte expansion. These distinct features differentiated affected mice into early, intermediate and advanced disease stages. Excessive tissue formation was observed in vertebral joints only if the IVD was destroyed as a consequence of the early inflammation. Ectopic excessive tissue was predominantly chondroidal with chondrocyte-like cells embedded within collagen type II- and X-rich matrix. This corresponded with upregulation of mRNA for cartilage markers Col2a1, sox9 and Comp. Osteophytes, though infrequent, were more prevalent in later disease.\ud \ud Conclusions\ud \ud The inflammation-driven IVD destruction was shown to be a prerequisite for axial disease progression to osteoproliferation in the PGISp mouse. Osteoproliferation led to vertebral body deformity and fusion but was never seen concurrent with persistent inflammation, suggesting a sequential process. The findings support that early intervention with anti-inflammatory therapies will be needed to limit destructive processes and consequently prevent progression of AS

Classification of hyperbolic Dynkin diagrams, root lengths and Weyl group orbits

We give a criterion for a Dynkin diagram, equivalently a generalized Cartan matrix, to be symmetrizable. This criterion is easily checked on the Dynkin diagram. We obtain a simple proof that the maximal rank of a Dynkin diagram of compact hyperbolic type is 5, while the maximal rank of a symmetrizable Dynkin diagram of compact hyperbolic type is 4. Building on earlier classification results of Kac, Kobayashi-Morita, Li and Sa\c{c}lio\~{g}lu, we present the 238 hyperbolic Dynkin diagrams in ranks 3-10, 142 of which are symmetrizable. For each symmetrizable hyperbolic generalized Cartan matrix, we give a symmetrization and hence the distinct lengths of real roots in the corresponding root system. For each such hyperbolic root system we determine the disjoint orbits of the action of the Weyl group on real roots. It follows that the maximal number of disjoint Weyl group orbits on real roots in a hyperbolic root system is 4.Comment: J. Phys. A: Math. Theor (to appear

On staying grounded and avoiding Quixotic dead ends

The 15 articles in this special issue on The Representation of Concepts illustrate the rich variety of theoretical positions and supporting research that characterize the area. Although much agreement exists among contributors, much disagreement exists as well, especially about the roles of grounding and abstraction in conceptual processing. I first review theoretical approaches raised in these articles that I believe are Quixotic dead ends, namely, approaches that are principled and inspired but likely to fail. In the process, I review various theories of amodal symbols, their distortions of grounded theories, and fallacies in the evidence used to support them. Incorporating further contributions across articles, I then sketch a theoretical approach that I believe is likely to be successful, which includes grounding, abstraction, flexibility, explaining classic conceptual phenomena, and making contact with real-world situations. This account further proposes that (1) a key element of grounding is neural reuse, (2) abstraction takes the forms of multimodal compression, distilled abstraction, and distributed linguistic representation (but not amodal symbols), and (3) flexible context-dependent representations are a hallmark of conceptual processing

Temporally stable coherent states in energy degenerate systems: The hydrogen atom

Klauder's recent generalization of the harmonic oscillator coherent states [J. Phys. A 29, L293 (1996)] is applicable only in non-degenerate systems, requiring some additional structure if applied to systems with degeneracies. The author suggests how this structure could be added, and applies the complete method to the hydrogen atom problem. To illustrate how a certain degree of freedom in the construction may be exercised, states are constructed which are initially localized and evolve semi-classically, and whose long time evolution exhibits "fractional revivals."Comment: 9 pages, 3 figure