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Biology subjects

Martin, K. L.

Publications and source records attributed to Martin, K. L..

2 recordsLinked to original sources

Mapping Coastal Forest Retreat Using Convolutional Neural Networks and Different Satellite Imagery

Coastal forests are increasingly threatened by saturated soil and elevated salinity levels resulting from sea level rise, saltwater intrusion, and storm surges. In response to rising salinization and flooding, healthy coastal forests that rely on freshwater (both wetland forests and low-elevation upland forests) are transitioning into landscapes dominated by dead or dying trees, known as ghost forests. Situated among salt-tolerant shrubs and grasses, ghost forests eventually become marshes or open water. Here, our main objective was to quantify the dynamics and pathways of these forest landscape conversions, as well as the factors contributing to the changes, which is vital for understanding the progression of coastal ecosystem degradation and forecasting future changes. We focused first on identifying the best method to track forest landscape change by exploring the role of multiple remote sensing indices (i.e., multispectral, bi-seasonal, topographical, and phenological metrics) in enhancing the performance of deep learning models (convolutional neural networks, CNNs) for land cover classification in the coastal plain of North Carolina using surface reflectance of Landsat 8 and Sentinel-2 images. Then, we used the best available data (Landsat 8) to understand long-term change and identify patterns of land cover change from 1985 to 2021. Our study reveals that incorporating phenology and topographical indices enhances the separability of the ghost forests class from all other vegetation classes. In our assessment, the higher-resolution Sentinel-2 data (F1 Score = 96.3) outperformed Landsat images (F1 score = 93.4) for the 2021 co-available year. However, Landsat remains an important tool used due to its long-term data record. Therefore, we used Landsat to determine that 21% of forests were lost between 1985 and 2021, and that the rate of loss is increasing. Between 2010 and 2021, 23,876 ha of forest were converted to marsh, ghost forest, and shrub, which is 1.5 times higher than the 16,968 ha lost between 1985 and 2010. These conversions from forest to ghost forest and marshes were driven primarily by proximity to the channel, salinity, and the increasing rate of relative sea level rise (RSLR), which are the key environmental drivers of observed changes. By quantifying these changes, we highlight regions most vulnerable to environmental stressors, providing a basis for targeted conservation strategies.

ecology↗

A mouse model of hemochromatosis-related mutations with brain iron dyshomeostasis exhibits loss of tyrosine hydroxylase expression in dopaminergic neurons and motor control impairment relevant to Parkinson's disease

UK Biobank studies show Parkinsons disease risk is almost doubled in men homozygous for the homeostatic iron regulator gene HFE p.C282Y polymorphism, associated with the common genetic iron disorder hemochromatosis. Whether this relationship is causal or spurious is unknown. We previously reported a novel Hfe-/-xTfr2mut mouse model of hemochromatosis with elevated brain iron ([~]1.5-1.8x). We now show these mice have reduced substantia nigra tyrosine hydroxylase expression at 3 months and 9 months age, sometimes exhibit severe hindlimb clasping by 7-8 months, have impaired rotarod and balance beam performance at 9 months and are untestable on the pole test. These parkinsonian features place the model at the forefront of genetic mouse models of PD, which generally do not show both TH loss and motor impairment. This confirms hemochromatosis-related mutations can cause parkinsonian features, substantiating causality of epidemiological relationships. Despite total brain iron elevation, neuronal iron remains low in Hfe-/-xTfr2mut mice, consistent with hemochromatosis-related mutations disrupting the normal, iron-responsive regulation of the neuronal iron exporter ferroportin by hepcidin. Parkinsonian features may reflect reduced mitochondrial respiratory complex (MRC) activity due to functional neuronal iron depletion. This may be exacerbated by indiscriminate chelation and could instead respond to drugs targeting the hepcidin-ferroportin axis or MRC activity. This new model of chronic parkinsonism that increases with age provides unprecedented insights into the complex relationships of brain iron regulation and movement impairment. Since parkinsonism of diverse etiologies can exhibit iron dysregulation, the model may facilitate pre-clinical to end-stage studies relevant to both sporadic and genetic PD.

neuroscience↗