The ecology of seamounts: structure, function, and human impacts.

In this review of seamount ecology, we address a number of key scientific issues concerning the structure and function of benthic communities, human impacts, and seamount management and conservation. We consider whether community composition and diversity differ between seamounts and continental slopes, how important dispersal capabilities are in seamount connectivity, what environmental factors drive species composition and diversity, whether seamounts are centers of enhanced biological productivity, and whether they have unique trophic architecture. We discuss how vulnerable seamount communities are to fishing and mining, and how we can balance exploitation of resources and conservation of habitat. Despite considerable advances in recent years, there remain many questions about seamount ecosystems that need closer integration of molecular, oceanographic, and ecological research

Analysis, Prevalence & Impact of Microplastics in Freshwater and Estuarine Environments Evidence Review 2 What are the sources of the microplastics found in freshwater environments?

This Rapid Evidence Assessment used the systematic review procedure to assess the current evidence available on the sources of the microplastics found in freshwater and estuarine environments. To fully comprehend the prevalence of microplastics in freshwater and estuarine environments, it is important to understand which sources contribute to the microplastics present and the relative importance of those sources. Furthermore, we need to understand the influence of any physical and biologically-mediated processes that affect the concentrations, characteristics and profile of the microplastic particles present, so that their influence can be taken into account when interpreting the microplastics present in terms of contributing sources. A review was conducted of literature, including grey literature, which reported evidence of the sources of the microplastics found in freshwater and estuarine environments. The factors influencing the transport and modification of microplastics in freshwater and estuarine environments were also considered, noting in particular those that alter the profile of microplastics thus obscuring identification of sources. Publications released prior to April 2019 were included in this review. Evidence was acquired according to a predefined set of questions, compiled into a database containing full details of the source and its relevance to the project questions, and the evidence analysed, taking into account reporting biases in the literature, to produce a digestible summary of the evidence base available to answer the main project question and sub-questions, namely, What are the sources of microplastics reported to have been found in freshwater and estuarine environments? a) Are these primary (i.e. manufactured) or secondary (i.e. degradation products) microplastics? b) Within studies reporting the predominant types of microplastics found, is there a link identified to local land use or industry? c) How are microplastics transported and modified in the freshwater and estuarine environments? d) Are microplastics from different sources prevalent in different matrices of the aquatic environment (biota, water, or sediment)

Evidence Reviews on Analysis, Prevalence & Impact of Microplastics in Freshwater and Estuarine Environments Evidence Review 3 What is/are the impact(s) of microplastics on freshwater and estuarine biota?

This Rapid Evidence Assessment used the systematic review procedure to assess the current evidence available on the impact of microplastics on freshwater and estuarine biota. It is important to understand what consequences microplastics may cause in the environment. Furthermore, we need to understand which types of microplastics cause impacts and at what concentrations. A review was conducted of the primary literature, including grey literature, which reported evidence of the impact of microplastics on freshwater and estuarine biota. A particular focus were those publications which reported evidence on the extent to which microplastics influence the behaviour, feeding, growth, reproduction and survival of freshwater and estuarine biota, and any thresholds at which impacts occurred. Publications released prior to April 2019 were included in this review. Evidence was acquired according to a predefined set of questions, compiled into a database containing full details of the source and its relevance to the project questions, and the evidence analysed, taking into account reporting biases in the literature, to produce a digestible summary of the evidence base available to answer the main project question and sub-questions, namely, What is/are the impact(s) of microplastics on freshwater and estuarine biota? a) To what extent do microplastics influence the feeding, growth, reproduction and survival of freshwater and estuarine biota? Do we know trigger levels or threshold values for microplastic impacts on biota? b) Are any differences between different taxonomic groups observed? c) Are results from laboratory studies relevant to microplastics at environmentally relevant field concentrations? d) Are any adverse impacts attributable to the particles or to adsorbed chemicals/microbes on the particles? e) Is there evidence to suggest impacts on populations of aquatic organisms

Blood test monitoring of immunomodulatory therapy in inflammatory disease

Practice Pointer article

Cyclooxygenase activity mediates colorectal cancer cell resistance to the omega-3 polyunsaturated fatty acid eicosapentaenoic acid

Purpose The naturally-occurring omega-3 polyunsaturated fatty acid eicosapentaenoic acid (EPA) is safe, well-tolerated and inexpensive, making it an attractive anti-cancer intervention. However, EPA has only modest anti-colorectal cancer (CRC) activity, when used alone. Both cyclooxygenase (COX) isoforms metabolise EPA and are over-expressed in CRC cells. We investigated whether COX inhibition increases the sensitivity of CRC cells to growth inhibition by EPA. Methods A panel of 18 human and mouse CRC cell lines was used to characterize the differential sensitivity of CRC cells to the growth inhibitory effects of EPA. The effect of CRISPR-Cas9 genetic deletion and pharmacological inhibition of COX-1 and COX-2 on the anti-cancer activity of EPA was determined using in vitro and in vivo models. Results Genetic ablation of both COX isoforms increased sensitivity of CT26 mouse CRC cells to growth inhibition by EPA in vitro and in vivo. The non-selective COX inhibitor aspirin and the selective COX-2 inhibitor celecoxib increased sensitivity of several human and mouse CRC cell lines to EPA in vitro. However, in a MC38 mouse CRC cell tumour model, with dosing that mirrored low-dose aspirin use in humans, thereby producing significant platelet COX-1 inhibition, there was ineffective intra-tumoral COX-2 inhibition by aspirin and no effect on EPA sensitivity of MC38 cell tumours. Conclusion Cyclooxygenase inhibition by non-steroidal anti-inflammatory drugs represents a therapeutic opportunity to augment the modest anti-CRC activity of EPA. However, intra-tumoral COX inhibition is likely to be critical for this drug-nutrient interaction and careful tissue pharmacodynamic profiling is required in subsequent pre-clinical and human studies

Performance of the Tariff Method: validation of a simple additive algorithm for analysis of verbal autopsies

<p>Abstract</p> <p>Background</p> <p>Verbal autopsies provide valuable information for studying mortality patterns in populations that lack reliable vital registration data. Methods for transforming verbal autopsy results into meaningful information for health workers and policymakers, however, are often costly or complicated to use. We present a simple additive algorithm, the Tariff Method (termed Tariff), which can be used for assigning individual cause of death and for determining cause-specific mortality fractions (CSMFs) from verbal autopsy data.</p> <p>Methods</p> <p>Tariff calculates a score, or "tariff," for each cause, for each sign/symptom, across a pool of validated verbal autopsy data. The tariffs are summed for a given response pattern in a verbal autopsy, and this sum (score) provides the basis for predicting the cause of death in a dataset. We implemented this algorithm and evaluated the method's predictive ability, both in terms of chance-corrected concordance at the individual cause assignment level and in terms of CSMF accuracy at the population level. The analysis was conducted separately for adult, child, and neonatal verbal autopsies across 500 pairs of train-test validation verbal autopsy data.</p> <p>Results</p> <p>Tariff is capable of outperforming physician-certified verbal autopsy in most cases. In terms of chance-corrected concordance, the method achieves 44.5% in adults, 39% in children, and 23.9% in neonates. CSMF accuracy was 0.745 in adults, 0.709 in children, and 0.679 in neonates.</p> <p>Conclusions</p> <p>Verbal autopsies can be an efficient means of obtaining cause of death data, and Tariff provides an intuitive, reliable method for generating individual cause assignment and CSMFs. The method is transparent and flexible and can be readily implemented by users without training in statistics or computer science.</p