Marine macroinvertebrate ecosystem services under changing conditions of seagrasses and mangroves.

This study aimed to investigate the impact of changing environmental conditions on MMI ES in seagrasses and mangroves. We used data from satellite and biodiversity platforms combined with field data to explore the links between ecosystem pressures (habitat conversion, overexploitation, climate change), conditions (environmental quality, ecosystem attributes), and MMI ES (provisioning, regulation, cultural). Both seagrass and mangrove extents increased significantly since 2016. While sea surface temperature showed no significant annual variation, sea surface partial pressure CO2, height above sea level and pH presented significant changes. Among the environmental quality variables only silicate, PO4 and phytoplankton showed significant annual varying trends. The MMI food provisioning increased significantly, indicating overexploitation that needs urgent attention. MMI regulation and cultural ES did not show significant trends overtime. Our results show that MMI ES are affected by multiple factors and their interactions can be complex and non-linear. We identified key research gaps and suggested future directions for research. We also provided relevant data that can support future ES assessments.

Downregulated Glia Interplay and Increased miRNA-155 as Promising Markers to Track ALS at an Early Stage.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of unknown cause. Absence of specific targets and biomarkers compromise the development of new therapeutic strategies and of innovative tools to stratify patients and assess their responses to treatment. Here, we investigate changes in neuroprotective-neuroinflammatory actions in the spinal cord of SOD1 G93A mice, at presymptomatic and symptomatic stages to identify stage-specific biomarkers and potential targets. Results showed that in the presymptomatic stage, there are alterations in both astrocytes and microglia, which comprise decreased expression of GFAP and S100B and upregulation of GLT-1, as well as reduced expression of CD11b, M2-phenotype markers, and a set of inflammatory mediators. Reduced levels of Connexin-43, Pannexin-1, CCL21, and CX3CL1 further indicate the existence of a compromised intercellular communication. In contrast, in the symptomatic stage, increased markers of inflammation became evident, such as NF-κB/Nlrp3-inflammasome, Iba1, pro-inflammatory cytokines, and M1-polarizion markers, together with a decreased expression of M2-phenotypic markers. We also observed upregulation of the CX3CL1-CX3CR1 axis, Connexin-43, Pannexin-1, and of microRNAs (miR)-124, miR-125b, miR-146a and miR-21. Reduced motor neuron number and presence of reactive astrocytes with decreased GFAP, GLT-1, and GLAST further characterized this inflammatory stage. Interestingly, upregulation of miR-155 and downregulation of MFG-E8 appear as consistent biomarkers of both presymptomatic and symptomatic stages. We hypothesize that downregulated cellular interplay at the early stages may represent neuroprotective mechanisms against inflammation, SOD1 aggregation, and ALS onset. The present study identified a set of inflamma-miRNAs, NLRP3-inflammasome, HMGB1, CX3CL1-CX3CR1, Connexin-43, and Pannexin-1 as emerging candidates and promising pharmacological targets that may represent potential neuroprotective strategies in ALS therapy.