Analysing and Applying Stakeholder Perceptions to Improve Protected Area Governance in Ugandan Conservation Landscapes

Given the diversity of active institutions and stakeholders in a landscape, and the difficulties in ensuring inclusive decision-making, evaluating landscape governance can help surface and address underlying issues. In the context of two protected area landscapes in Uganda, where landscape approaches are being implemented through a wider project on landscape governance, we analyse stakeholder perceptions of inclusive decision-making and then use this evaluation to stimulate dialogue amongst stakeholder groups in each landscape. We ask, how can capturing, analysing, and collaboratively applying people’s perceptions address inclusive decision-making in landscape governance? We collected and analysed perceptions using SenseMaker®, a software package that enables analysis of micronarratives (stories) from the field based on how respondents classify their own stories, using triads, dyads, stones, and multiple-choice questions. This self-categorisation by the respondent reduces bias in the analysis and allows the micronarrative to be cross-examined in a variety of ways when analysed using Sensemaker. This analysis created an integrated view of the stakeholder’s perceptions about inclusive decision-making in landscape governance. The results show large portions of the respondents feel their voices are neglected, and management of the landscape is poor in Mount Elgon, while in Agoro-Agu, it is the opposite trend. During a community feedback process, reasons for these trends were discussed and solutions proposed. Some of the underlying factors include historical relationships with park authorities and displacement during park creation. To more precisely answer our research question, one could have extended stays in the communities studied in these landscapes, using ethnographic methods including interviews and participant observation; nonetheless, our method, including the feedback process, was an innovative and important way to confront our findings with the informants directly and foster collaborative action. We conclude that understanding people’s perceptions, including through participatory feedback, can significantly inform and improve management decisions, help resolve conflicts, and facilitate dialogue between different stakeholders in the landscape

Difference in Mono-O-Glucosylation of Ras Subtype GTPases Between Toxin A and Toxin B From Clostridioides difficile Strain 10463 and Lethal Toxin From Clostridium sordellii Strain 6018

Clostridioides difficile toxin A (TcdA) and Toxin B (TcdB) trigger inflammasome activation with caspase-1 activation in cultured cells, which in turn induce the release of IL-6, IFN-γ, and IL-8. Release of these proinflammatory responses is positively regulated by Ras-GTPases, which leads to the hypothesis that Ras glucosylation by glucosylating toxins results in (at least) reduced proinflammatory responses. Against this background, data on toxin-catalyzed Ras glucosylation are required to estimate of pro-inflammatory effect of the glucosylating toxins. In this study, a quantitative evaluation of the GTPase substrate profiles glucosylated in human colonic (Caco-2) cells treated with either TcdA, TcdB, or the related Clostridium sordellii lethal toxin (TcsL) was performed using multiple reaction monitoring (MRM) mass spectrometry. (H/K/N)Ras are presented to be glucosylated by TcsL and TcdA but by neither TcdB isoform tested. Furthermore, the glucosylation of (H/K/N)Ras was detected in TcdA-(not TcdB)-treated cells, as analyzed exploiting immunoblot analysis using the Ras glucosylation-sensitive 27H5 antibody. Furthermore, [14C]glucosylation of substrate GTPase was found to be increased in a cell-free system complemented with Caco-2 lysates. Under these conditions, (H/K/N)Ras glucosylation by TcdA was detected. In contrast, TcdB-catalyzed (H/K/N)Ras glucosylation was detected by neither MRM analysis, immunoblot analysis nor [14C]glucosylation in a cell-free system. The observation that TcdA (not TcdB) glucosylates Ras subtype GTPases correlates with the fact that TcdB (not TcdA) is primarily responsible for inflammatory responses in CDI. Finally, TcsL more efficaciously glucosylated Ras subtype GTPase as compared with TcdA, reinforcing the paradigm that TcsL is the prototype of a Ras glucosylating toxin