TRY plant trait database - enhanced coverage and open access

Plant traits-the morphological, anatomical, physiological, biochemical and phenological characteristics of plants-determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait-based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits-almost complete coverage for 'plant growth form'. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait-environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Pengantar tentang kriminologi

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Efeitos comportamentais, cognitivos e psicofisiológicos dos canabinoides: relevância para a psicose e a esquizofrenia Behavioral, cognitive and psychophysiological effects of cannabinoids: relevance to psychosis and schizophrenia

Avanços recentes no conhecimento sobre a função do receptor de canabinoide renovaram o interesse na associação entre cannabis e psicose. Linhas convergentes de evidências sugerem que os canabinoides podem produzir uma ampla gama de sintomas transitórios positivos, negativos e cognitivos assemelhados aos de esquizofrenia. Os canabinoides também produzem alguns déficits psicofisiológicos sabidamente presentes na esquizofrenia. É igualmente claro que em indivíduos com um transtorno psicótico estabelecido, os canabinoides podem exacerbar sintomas, desencadear recaídas e ter consequências negativas no curso da doença. Evidências crescentes sugerem que a exposição precoce e pesada à cannabis pode aumentar o risco de se desenvolver um transtorno psicótico como a esquizofrenia. A relação entre exposição à cannabis e esquizofrenia preenche alguns, mas não todos os critérios usuais de causalidade. Porém, a maioria das pessoas que utilizam cannabis não desenvolve esquizofrenia e muitas pessoas diagnosticadas com esquizofrenia nunca utilizaram cannabis. Portanto, é provável que a exposição à cannabis seja uma "causa componente" que interage com outros fatores para "causar" esquizofrenia ou outro transtorno psicótico, mas não é nem necessária nem suficiente para fazê-lo sozinha. No entanto, na ausência de causas conhecidas da esquizofrenia e com as implicações de políticas de saúde pública, se tal vínculo for estabelecido, as causas componentes, tais como a exposição a canabinoide, devem continuar sendo um foco de estudos futuros. Finalmente, são necessárias mais pesquisas para identificar os fatores subjacentes à vulnerabilidade à psicose relacionada a canabinoide e para elucidar os mecanismos biológicos subjacentes a esse risco.<br>Recent advances in knowledge about cannabinoid receptor function have renewed interest in the association between cannabis and psychosis. Converging lines of evidence suggest that cannabinoids can produce a full range of transient schizophrenia-like positive, negative and cognitive symptoms. Cannabinoids also produce some psychophysiological deficits also known to be present in schizophrenia. Also clear is that in individuals with an established psychotic disorder, cannabinoids can exacerbate symptoms, trigger relapse, and have negative consequences on the course of the illness. Increasing evidence suggests that early and heavy cannabis exposure may increase the risk of developing a psychotic disorder such as schizophrenia. The relationship between cannabis exposure and schizophrenia fulfills some, but not all, of the usual criteria for causality. However, most people who use cannabis do not develop schizophrenia, and many people diagnosed with schizophrenia have never used cannabis. Therefore, it is likely that cannabis exposure is a "component cause" that interacts with other factors to "cause" schizophrenia or other psychotic disorder, but is neither necessary nor sufficient to do so alone. In the absence of known causes of schizophrenia, however, and the implications for public health policy should such a link be established the role of component causes such as cannabinoid exposure should remain a focus of further study. Finally, further work is necessary to identify the factors that underlie individual vulnerability to cannabinoid-related psychosis and to elucidate the biological mechanisms underlying this risk