Food for pollinators: quantifying the nectar and pollen resources of urban flower meadows

Planted meadows are increasingly used to improve the biodiversity and aesthetic amenity value of urban areas. Although many ‘pollinator-friendly’ seed mixes are available, the floral resources these provide to flower-visiting insects, and how these change through time, are largely unknown. Such data are necessary to compare the resources provided by alternative meadow seed mixes to each other and to other flowering habitats. We used quantitative surveys of over 2 million flowers to estimate the nectar and pollen resources offered by two exemplar commercial seed mixes (one annual, one perennial) and associated weeds grown as 300m2 meadows across four UK cities, sampled at six time points between May and September 2013. Nectar sugar and pollen rewards per flower varied widely across 65 species surveyed, with native British weed species (including dandelion, Taraxacum agg.) contributing the top five nectar producers and two of the top ten pollen producers. Seed mix species yielding the highest rewards per flower included Leontodon hispidus, Centaurea cyanus and C. nigra for nectar, and Papaver rhoeas, Eschscholzia californica and Malva moschata for pollen. Perennial meadows produced up to 20x more nectar and up to 6x more pollen than annual meadows, which in turn produced far more than amenity grassland controls. Perennial meadows produced resources earlier in the year than annual meadows, but both seed mixes delivered very low resource levels early in the year and these were provided almost entirely by native weeds. Pollen volume per flower is well predicted statistically by floral morphology, and nectar sugar mass and pollen volume per unit area are correlated with flower counts, raising the possibility that resource levels can be estimated for species or habitats where they cannot be measured directly. Our approach does not incorporate resource quality information (for example, pollen protein or essential amino acid content), but can easily do so when suitable data exist. Our approach should inform the design of new seed mixes to ensure continuity in floral resource availability throughout the year, and to identify suitable species to fill resource gaps in established mixes

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

Paclitaxel and beta-lapachone synergistically induce apoptosis in human retinoblastoma Y79 cells by downregulating the levels of phospho-Akt.

Paclitaxel (PTX) and beta-lapachone (LPC) are naturally occurring compounds that have shown a large spectrum of anticancer activity. In this article we show for the first time that PTX/LPC combination induces potent synergistic apoptotic effects in human retinoblastoma Y79 cells. Combination of suboptimal doses of PTX (0.3 nM) and LPC (1.5 microM) caused biochemical and morphological signs of apoptosis at 48 h of treatment. These effects were accompanied by potent lowering in inhibitor of apoptosis proteins and by activation of Bid and caspases 3 and 6 with lamin B and PARP breakdown. PTX/LPC combination acted by favoring p53 stabilization through a lowering in p-Akt levels and in ps166-MDM2, the phosphorylated-MDM2 form that enters the nucleus and induces p53 export and degradation. Treatment with wortmannin or transfection with a dominant negative form of Akt anticipated at 24 h the effects induced by PTX/LPC, suggesting a protective role against apoptosis played by Akt in Y79 cells. In line with these results, we demonstrated that Y79 cells contain constitutively active Akt, which forms a cytosolic complex with p53 and MDM2 driving p53 degradation. PTX/LPC treatment induced a weakness of Akt-MDM2-p53 complex and increased nuclear p53 levels. Our results suggest that phospho-Akt lowering is at the root of the apoptotic action exerted by PTX/LPC combination and provide strong validation for a treatment approach that targets survival signals represented by phospho-Akt and inhibitor of apoptosis proteins

Acurácia do exame clínico no diagnóstico da DPOC Accuracy of clinical examination findings in the diagnosis of COPD

OBJETIVO: A DPOC é um problema de saúde pública, e métodos diagnósticos simples podem ser úteis para facilitar o diagnóstico desta doença. O objetivo deste estudo foi avaliar a acurácia de variáveis clínicas para o diagnóstico de DPOC. MÉTODOS: Pacientes com DPOC e controles foram prospectivamente avaliados por dois examinadores quanto a nove variáveis clínicas. A razão de verossimilhança para o diagnóstico de DPOC foi determinada utilizando-se o modelo de regressão logística. RESULTADOS: Foram incluídos 98 pacientes com DPOC (idade média, 62,3 ± 12,3 anos; VEF1 médio, 48,3 ± 21,6%) e 102 controles. A razão de verossimilhança e IC95% para o diagnóstico de DPOC foram: 4,75 (2,29-9,82; p < 0,0001) para uso da musculatura acessória; 5,05 (2,72-9,39; p < 0,0001) para respiração com os lábios semicerrados; 2,58 (1,45-4,57; p < 0,001) para tórax em barril; 3,65 (2,01-6,62; p < 0,0001) para redução da expansibilidade torácica; 7,17 (3,75-13,73; p < 0,0001) para redução do murmúrio vesicular; 2,17 (1,01-4,67; p < 0,05) para índice torácico > 0,9; 2,36 (1,22-4,58; p < 0,05) para comprimento laríngeo < 5,5 cm; 3,44 (1,92-6,16; p < 0,0001) para tempo expiratório forçado > 4 s; e 4,78 (2,13-10,70; p < 0.0001) para limite inferior do fígado > 4 cm abaixo do rebordo costal. A concordância entre observadores para as mesmas variáveis foi, respectivamente, 0,57, 0,45, 0,62, 0,32, 0,53, 0,32, 0,59, 0,52 e 0,44 (p < 0,0001 para todas). CONCLUSÕES: Vários achados do exame clínico podem ser utilizados como testes diagnósticos para DPOC.<br>OBJECTIVE: Simple diagnostic methods can facilitate the diagnosis of COPD, which is a major public health problem. The objective of this study was to investigate the accuracy of clinical variables in the diagnosis of COPD. METHODS: Patients with COPD and control subjects were prospectively evaluated by two investigators regarding nine clinical variables. The likelihood ratio for the diagnosis of COPD was determined using a logistic regression model. RESULTS: The study comprised 98 patients with COPD (mean age, 62.3± 12.3 years; mean FEV1, 48.3 ± 21.6%) and 102 controls. The likelihood ratios (95% CIs) for the diagnosis of COPD were as follows: 4.75 (2.29-9.82; p < 0.0001) for accessory muscle recruitment; 5.05 (2.72-9.39; p < 0.0001) for pursed-lip breathing; 2.58 (1.45-4.57; p < 0.001) for barrel chest; 3.65 (2.01-6.62; p < 0.0001) for decreased chest expansion; 7.17 (3.75-13.73; p < 0.0001) for reduced breath sounds; 2.17 (1.01-4.67; p < 0.05) for a thoracic index > 0.9; 2.36 (1.22-4.58; p < 0.05) for laryngeal height < 5.5 cm; 3.44 (1.92-6.16; p < 0.0001) for forced expiratory time > 4 s; and 4.78 (2.13-10.70; p < 0.0001) for lower liver edge > 4 cm from lower costal edge. Inter-rater reliability for those same variables was, respectively, 0.57, 0.45, 0.62, 0.32, 0.53, 0.32, 0.59, 0.52 and 0.44 (p < 0.0001 for all). CONCLUSIONS: Various clinical examination findings could be used as diagnostic tests for COPD