An Ecosystem Framework for use in Recovery and Management of the Puget Sound Ecosystem: Linking Assessments of Ecosystem Condition to Threats and Management Strategies

The ongoing influx of people to the Puget Sound basin has placed pressure on the ecosystem and contributed to a decline in ecosystem health. The Puget Sound Partnership (Partnership), formed in July 2007, is leading an effort to restore the health of Puget Sound. The Partnership is taking an ecosystem-based approach to management that will, over time, address policy questions associated with multiple interacting ecosystem goals. As a foundation of this approach, indicators of ecosystem condition are used to describe a healthy Puget Sound, to evaluate progress towards meeting the recovery goals, to evaluate and adapt management strategies, and as the basis for reporting back to the public. A portfolio of high-level ecological and human health indicators, “vital signs,” was developed and adopted in 2011. Since then, the indicators have received external review by the WA State Academy of Sciences, scientists, planners, decision-makers, and other stakeholders. In response, the Partnership is evolving its portfolio of indicators in order to provide a broader set of indicators to track progress toward threat reductions and ecosystem recovery. To guide the indicator evolution process, we developed an overall organizing ecosystem framework that is an amalgamation of three frameworks: (1) a generalized “causal chain/network framework” that is used to link drivers and pressures of ecosystem health with (2) a framework for assessment of the condition of Puget Sound’s biophysical system, and (3) a framework for the condition of human well-being (HWB). Assessing a complete array of condition and driver/pressure indicators can aid the analysis of the causal mechanisms underlying compromised ecosystem condition. Moreover, in this framework, HWB is recognized as an outcome of biophysical condition as well as a driver of biophysical condition, and that its many components are differentially affected by and can affect conservation outcomes. This paper will present examples of how the Partnership, working with the Puget Sound Ecosystem Monitoring Program, is using this ecosystem framework to identify key ecosystem attributes and associated indicators for major ecosystem components. These biophysical condition indicators, along with indicators of key pressures on the system and indicators of HWB, can be used adaptively to track the recovery of Puget Sound

Navigating spaces between conservation research and practice: are we making progress?

1. Despite aspirations for conservation impact, mismatches between research and implementation have limited progress towards this goal. There is, therefore, an urgent need to identify how we can more effectively navigate the spaces between research and practice. 2. In 2014, we ran a workshop with conservation researchers and practitioners to identify mismatches between research and implementation that needed to be overcome to deliver evidence‐informed conservation action. Five mismatches were highlighted: spatial, temporal, priority, communication, and institutional. 3. Since 2014, thinking around the ‘research–implementation gap’ has progressed. The term ‘gap’ has been replaced by language around the dynamic ‘spaces’ between research and action, representing a shift in thinking around what it takes to better align research and practice. 4. In 2019, we ran a follow‐up workshop reflecting on this shift, whether the five mismatches identified in the 2014 workshop were still present in conservation, and whether progress had been made to overcome these mismatches during the past 5 years. We found that while there has been progress, we still have some way to go across all dimensions. 5. Here, we report on the outcomes of the 2019 workshop, reflect on what has changed over the past 5 years, and offer 10 recommendations for strengthening the alignment of conservation research and practice

Design and Deploying Tools to ‘Actively Engaging Nature’: The My Naturewatch Project as an Agent for Engagement

‘Shifting Baseline Syndrome’ is highly apparent in the context of generational shifts in work and life patterns that reduce interaction with and knowledge of the natural world, and therefore expectations of it. This is exacerbated by changes in the natural world itself due to climate change, biodiversity decline and a range of anthropogenic factors. Distributed and accessible technologies, and grass roots approaches provide fresh opportunities for interactions, which enable active engagement in ecological scenarios. The My NatureWatch project uses digital devices to collect visual content about UK wildlife, promoting ‘active engagements with nature’. The project embodies Inclusive Design in the Digital Age, as the activity; engages a wide demographic community, can be used by all, provided user led agency and produced methodological design lessons. The article frames My Naturewatch as an agent for active designed engagements with nature. The research objective is to comprehend ‘how to design tools for positive nature engagement’ holding value for; (1) academic communities as validated methodologies (2) the public through access to enabling technologies, content and knowledge (3) industry in the form of new; experiences, engagements and commerce. The approach is specifically designed to yield insights from a multitude of engagements, through the deployment of accessible, lowcost products. Project reporting documents the benefits, pitfalls and opportunities in the aforementioned engagement uncovered through design-led approaches. Insights are gathered from public/community facing workshops, wildlife experts, ecologists, economists, educators and wildlife NGO’s. The engagement methodologies are compared highlighting which initiative yielded ‘Active Engagement with Nature’

Inhibition of the NLRP3/IL-1β axis protects against sepsis-induced cardiomyopathy

BACKGROUND: Septic cardiomyopathy worsens the prognosis of critically ill patients. Clinical data suggest that interleukin-1β (IL-1β), activated by the NLRP3 inflammasome, compromises cardiac function. Whether or not deleting Nlrp3 would prevent cardiac atrophy and improve diastolic cardiac function in sepsis was unclear. Here, we investigated the role of NLRP3/IL-1β in sepsis-induced cardiomyopathy and cardiac atrophy. METHODS: Male Nlrp3 knockout (KO) and wild-type (WT) mice were exposed to polymicrobial sepsis by caecal ligation and puncture (CLP) surgery (KO, n = 27; WT, n = 33) to induce septic cardiomyopathy. Sham-treated mice served as controls (KO, n = 11; WT, n = 16). Heart weights and morphology, echocardiography and analyses of gene and protein expression were used to evaluate septic cardiomyopathy and cardiac atrophy. IL-1β effects on primary and immortalized cardiomyocytes were investigated by morphological and molecular analyses. IonOptix and real-time deformability cytometry (RT-DC) analysis were used to investigate functional and mechanical effects of IL-1β on cardiomyocytes. RESULTS: Heart morphology and echocardiography revealed preserved systolic (stroke volume: WT sham vs. WT CLP: 33.1 ± 7.2 μL vs. 24.6 ± 8.7 μL, P < 0.05; KO sham vs. KO CLP: 28.3 ± 8.1 μL vs. 29.9 ± 9.9 μL, n.s.; P < 0.05 vs. WT CLP) and diastolic (peak E wave velocity: WT sham vs. WT CLP: 750 ± 132 vs. 522 ± 200 mm/s, P < 0.001; KO sham vs. KO CLP: 709 ± 152 vs. 639 ± 165 mm/s, n.s.; P < 0.05 vs. WT CLP) cardiac function and attenuated cardiac (heart weight-tibia length ratio: WT CLP vs. WT sham: -26.6%, P < 0.05; KO CLP vs. KO sham: -3.3%, n.s.; P < 0.05 vs. WT CLP) and cardiomyocyte atrophy in KO mice during sepsis. IonOptix measurements showed that IL-1β decreased contractility (cell shortening: IL-1β: -15.4 ± 2.3%, P < 0.001 vs. vehicle, IL-1RA: -6.1 ± 3.3%, P < 0.05 vs. IL-1β) and relaxation of adult rat ventricular cardiomyocytes (time-to-50% relengthening: IL-1β: 2071 ± 225 ms, P < 0.001 vs. vehicle, IL-1RA: 564 ± 247 ms, P < 0.001 vs. IL-1β), which was attenuated by an IL-1 receptor antagonist (IL-1RA). RT-DC analysis indicated that IL-1β reduced cardiomyocyte size (P < 0.001) and deformation (P < 0.05). RNA sequencing showed that genes involved in NF-κB signalling, autophagy and lysosomal protein degradation were enriched in hearts of septic WT but not in septic KO mice. Western blotting and qPCR disclosed that IL-1β activated NF-κB and its target genes, caused atrophy and decreased myosin protein in myocytes, which was accompanied by an increased autophagy gene expression. These effects were attenuated by IL-1RA. CONCLUSIONS: IL-1β causes atrophy, impairs contractility and relaxation and decreases deformation of cardiomyocytes. Because NLRP3/IL-1β pathway inhibition attenuates cardiac atrophy and cardiomyopathy in sepsis, it could be useful to prevent septic cardiomyopathy

Socio-cultural dimensions of marine spatial planning

Bringing together the complex social and cultural dimensions of marine spatial planning (MSP), this chapter examines how these two terms are applied (or not) in the context of MSP. Global marine and coastal planning continues to recognise that human activities must be considered in order to account for the dynamic interconnectivity between society and the sea. Many research fields explore the importance of the sea to identity, sense of place, health or community cohesion. However, these draw on a range of different assumptions to mainstream marine science and struggle to be incorporated into traditional policy processes, environmental assessments and large-scale planning processes. In this chapter, we interrogate the concept of ‘socio-cultural’, examining how this is being defined and applied across the MSP landscape

Graduate students and knowledge exchange with local stakeholders: possibilities and preparation

Tropical biologists are exploring ways to expand their role as researchers through knowledge exchange with local stakeholders. Graduate students are well positioned for this broader role, particularly when supported by graduate programs. We ask: (1) how can graduate students effectively engage in knowledge exchange during their research; and (2) how can university programs prepare young scientists to take on this partnership role? We present a conceptual framework with three levels at which graduate students can exchange knowledge with stakeholders (information sharing, skill building, and knowledge generation) and discuss limitations of each. Examples of these strategies included disseminating preliminary research results to southern African villages, building research skills of Brazilian undergraduate students through semester-long internships, and jointly developing and implementing a forest ecology research and training program with one community in the Amazon estuary. Students chose strategies based on stakeholders' interests, research goals, and a realistic evaluation of student capacity and skill set. As strategies became more complex, time invested, skills mobilized, and strength of relationships between students and stakeholders increased. Graduate programs can prepare students for knowledge exchange with partners by developing specialized skills training, nurturing external networks, offering funding, maximizing strengths of universities in developed and developing regions through partnership, and evaluating knowledge exchange experiences. While balancing the needs of academia with those of stakeholders is challenging, the benefits of enhancing local scientific capacity and generating more locally relevant research for improved conservation may be worth the risks associated with implementing this type of graduate training model

PIEZO1-mediated mechanosensing governs NK cell killing efficiency and infiltration in three-dimensional matrices

Natural killer (NK) cells play a vital role in eliminating tumorigenic cells. Efficient locating and killing of target cells in complex three-dimensional (3D) environments are critical for their functions under physiological conditions. However, the role of mechanosensing in regulating NK cell killing efficiency in physiologically relevant scenarios is poorly understood. Here, we report that the responsiveness of NK cells is regulated by tumor cell stiffness. NK cell killing efficiency in 3D is impaired against softened tumor cells, while it is enhanced against stiffened tumor cells. Notably, the durations required for NK cell killing and detachment are significantly shortened for stiffened tumor cells. Furthermore, we have identified PIEZO1 as the predominantly expressed mechanosensitive ion channel among the examined candidates in NK cells. Perturbation of PIEZO1 abolishes stiffness-dependent NK cell responsiveness, significantly impairs the killing efficiency of NK cells in 3D, and substantially reduces NK cell infiltration into 3D collagen matrices. Conversely, PIEZO1 activation enhances NK killing efficiency as well as infiltration. In conclusion, our findings demonstrate that PIEZO1-mediated mechanosensing is crucial for NK killing functions, highlighting the role of mechanosensing in NK cell killing efficiency under 3D physiological conditions and the influence of environmental physical cues on NK cell functions

PIEZO1-mediated mechanosensing governs NK-cell killing efficiency and infiltration in three-dimensional matrices

Natural killer (NK) cells play a vital role in eliminating tumorigenic cells. Efficient locating and killing of target cells in complex three-dimensional (3D) environments are critical for their functions under physiological conditions. However, the role of mechanosensing in regulating NK-cell killing efficiency in physiologically relevant scenarios is poorly understood. Here, we report that the responsiveness of NK cells is regulated by tumor cell stiffness. NK-cell killing efficiency in 3D is impaired against softened tumor cells, whereas it is enhanced against stiffened tumor cells. Notably, the durations required for NK-cell killing and detachment are significantly shortened for stiffened tumor cells. Furthermore, we have identified PIEZO1 as the predominantly expressed mechanosensitive ion channel among the examined candidates in NK cells. Perturbation of PIEZO1 abolishes stiffness-dependent NK-cell responsiveness, significantly impairs the killing efficiency of NK cells in 3D, and substantially reduces NK-cell infiltration into 3D collagen matrices. Conversely, PIEZO1 activation enhances NK killing efficiency as well as infiltration. In conclusion, our findings demonstrate that PIEZO1-mediated mechanosensing is crucial for NK killing functions, highlighting the role of mechanosensing in NK-cell killing efficiency under 3D physiological conditions and the influence of environmental physical cues on NK-cell functions