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Coral reefs are highly diverse ecosystems that provide many goods and ecosystem services globally. Coral reef ecosystems are also threatened by environmental stressors from anthropogenic sources and shifting climates. The United Nations Sustainable Development Goal 14 (“Life Below Water”) addresses the need to conserve and sustainably use the ocean, seas, and marine ecosystems, including reef systems. Belize’s coral reef system is the second largest in the world, providing sources of income to Belizeans through tourism and fisheries as well as coastline protection. In order to conserve their marine ecosystems, Belize has a network of Marine Protected Areas (MPAs) throughout their coastal waters. Using Aqua MODIS satellite imagery from 2002 to 2022, Google Earth Engine, and RStudio, we present a workflow to calculate stress days on MPAs and a coral vulnerability index based on sea surface temperature (SST) and Kd (490), a proxy of water clarity. The Corozal Bay, Swallow Caye, Port Honduras, and South Water Caye MPAs had the highest percentages of stress days and coral vulnerability stress index score based on these two parameters among the 24 MPAs analyzed. Additionally, SST in the warmest month of the year in Belize were seen to increase across all MPAs from 2002 to 2022 (p < 0.01). This GEE toolkit provides a straightforward and accessible tool to help governments monitor both water quality and risks to coral reefs in accordance with SDG 14.

Objective Cerebrospinal fluid (CSF) and plasma neurofilament light (NFL) concentrations were assessed in relation to longitudinal objective and subjective cognitive outcomes in older adults ranging from normal cognition to mild cognitive impairment. Interactive effects were assessed for apolipoprotein E ϵ4 (APOE4) carriership, a strong genetic risk factor for Alzheimer’s disease and molecular moderator of vascular disease. Method Vanderbilt Memory & Aging Project participants (CSF n = 149, 72 ± 6 years; plasma n = 333, 73 ± 7 years) underwent fasting blood draw and lumbar puncture at baseline for NFL quantification. Serial neuropsychological assessments and subjective cognitive decline (SCD) questionnaires were completed at 18-month increments. Linear mixed effects regression models adjusted for age, sex, race/ethnicity, education, APOE4 carriership (for main effect models), and depressed mood. NFL x APOE4 interaction terms were used as predictors in follow-up models. Results CSF NFL predicted steeper declines in an executive functioning composite score (β = −0.0001, p = 0.001) and WAIS-IV Coding (β = −0.001, p = 0.001). An APOE4 interaction was present for executive functioning (β = −0.0002, p = 0.005) such that CSF NFL associations with longitudinal decline were stronger among APOE4+ participants. Plasma NFL predicted worsening SCD (β = 0.27, p = 0.002) and objective cognitive decline across all domains (p-values Conclusions Both CSF and plasma NFL detect neuropathology associated with cognitive decline among non-demented older adults, especially among APOE4 carriers. Findings further support the value of SCD as reflecting neurodegenerative changes associated with accelerated cognitive aging.

Objective Subjective cognitive decline (SCD), a potential precursor to Alzheimer’s disease (ad), has been associated with increased neurodegeneration and cerebrovascular disease longitudinally. However, the impact of amyloid status, an early pathological marker of Alzheimer’s disease (ad) on these longitudinal associations is less clear. Here, we related baseline SCD to longitudinal biomarkers of brain health in the context of amyloid status. Method Participants included 139 non-demented older adults (72 ± 7 years) from the Vanderbilt Memory & Aging Project who completed a SCD questionnaire and fasting lumbar-puncture to quantify amyloid status (defined using published cutoffs of amyloid-beta42 levels) at baseline. 3 T brain-MRI to measure gray and white matter hyperintensity (WMH) volumes was collected at baseline, 18-months, 3-years, and 5-years. Linear mixed effects models assessed if baseline SCD X amyloid status was associated with longitudinal total and lobar grey and white matter volumes, covarying for baseline age, sex, race/ethnicity, education, diagnosis, mood, and apolipoprotein-Ee4 status. Models were also stratified by baseline amyloid status. Results Baseline SCD score and amyloid status interacted with total gray (p = 0.02) and WMH volume (p Conclusion In the presence of amyloid, the presence of SCD is predictive of neurodegeneration in ad-specific regions. Conversely, SCD without amyloidosis may reflect a cerebrovascular disease, indicated by WMHs. Results highlight how amyloid status may help delineate etiologies of SCD.

Objective Neurogranin is a postsynaptic protein associated with declining memory and executive functioning in Alzheimer’s disease (ad). While previous research suggests neurogranin concentrations in ad are higher in women, it is unclear whether sex differences exist in earlier disease stages or predict different cognitive outcomes. This study investigates cerebrospinal fluid (CSF) neurogranin in relation to longitudinal cognitive decline in older adults ranging from normal cognition to mild cognitive impairment, assessing for interactions by sex. Method Vanderbilt Memory & Aging Project participants completed baseline fasting lumbar puncture (n = 155, 73 ± 8 years) for neurogranin quantification and serial neuropsychological assessments at 18-month intervals. Linear mixed effect regression adjusting for age, sex (for main effect models), race/ethnicity, education, cognitive diagnosis, depressed mood, and APOE-ε4 carrier status. Results CSF neurogranin predicted worse cognitive decline across multiple domains (p-values Conclusion Results suggest that among nondemented older adults, CSF neurogranin predicts worse longitudinal cognitive decline in women but not in men. Further research is needed to elucidate underlying mechanisms that may account for these differences, such as possible sex hormone factors. These findings highlight the importance of pursuing individualized prevention and treatment approaches to combat accelerated cognitive aging that take into account the possibility of multiple, divergent disease pathways preceding ad and dementia among various demographic groups.

This interlude situates Dibdin in a milieu that may surprise us today, but that was a key comparison to many contemporaries: that is, alongside rural labouring-class poets, with particular emphasis on Robert Bloomfield. Rather than revisit Raymond Williams (who spares only two pages for Bloomfield in The Country and the City and ignores Dibdin), it interrogates the intersection of metropolis and countryside by locating these two writers’ texts within their working lives, networks, and practices, their music, and their engagement with particular London audiences. These active, commercial, humorous performers are contrasted to the antiquarian idealism of Percy and others, offering a reading of the rustic and the citizen that is knowing, even-handed, and modern.