126 research outputs found

    How Transient Patches Affect Population Dynamics: The Case of Hypoxia and Blue Crabs

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    Transient low-oxygen patches may have important consequences for the population dynamics of estuarine species. We investigated whether these transient hypoxic patches altered population dynamics of the commercially important blue crab (Callinectes sapidus) and assessed two alternative hypotheses for the causal mechanism. One hypothesis is that temporary reductions in habitat due to hypoxia increase cannibalism. The second hypothesis is that crab population dynamics result from food limitation caused by hypoxia-induced mortality of the benthos. We developed a spatially explicit individual-based model of blue crabs in a hierarchical framework to connect the autoecology of crabs with the spatial and temporal dynamics of their physical and biological environments. Three primary scenarios were run to examine the interactive effects of (1) hypoxic extent vs. static and transient patches, (2) hypoxic extent vs. prey abundance, and (3) hypoxic extent vs. cannibalism potential. Static patches resulted in populations limited by egg production and recruitment whereas transient patches led to populations limited by the effects of cannibalism and patch interactions. Crab survivorship was greatest for simulations with the largest hypoxic patches which also had the lowest prey abundance and lowest crab densities. In these simulations, nearly all crab mortality was accounted for by aggression, not starvation. In addition, increased prey abundance had little influence on crab abundance and dynamics, and massive reductions in prey abundance (\u3e 50%) were necessary to decrease crab abundance, survival, and egg production. Our analyses suggest that cannibalism coupled with decreased egg production determined key aspects of crab demography. Specifically, decreased cannibalism potential resulted in a food-limited crab population with long development times and high adult crab densities whereas increased cannibalism potential led to low adult crab densities with higher individual egg production rates. Our analyses identified several key knowledge gaps, including the nature of crab-crab cannibalism and the role of refuges from predation. Several experiments are suggested to test model predictions and to improve understanding of ecosystem-population linkages for this estuarine species

    The Lantern Vol. 51, No. 1, Fall 1984

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    • Sky Eyes • Flowerwait • Haiku • Sunwatch • Epitaph of A Tale • How Do You Tell A Child • Vineyard Wind • By The Sea • The Wanderer • In Back of the Real Supermarket in Collegeville • Mitosis • Smoke Dreams • On Humankind Today - A Message • Dragon • The Lull • Finale • The Sun • Three Steps in Life • Seaside • To Mark • To Father • Yesterday - Today • The Stars • The Journey • Our Shared Experience, Miles Away • Coming Home • Blossom • Life is the Teacher • Midnight Stroll in February • Eyes (Karen\u27s Poem) • Your Love • Same Welcome as Odysseus • Europa • Sinn Fein • Idle Dreams • I Can Take A Hint • In Retrospect • Rest • China and Porcelain are One in the Same • Momenthttps://digitalcommons.ursinus.edu/lantern/1125/thumbnail.jp

    Baseline microglial activation correlates with brain amyloidosis and longitudinal cognitive decline in Alzheimer disease

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    BACKGROUND AND OBJECTIVES: This study aims to quantify microglial activation in individuals with Alzheimer disease (AD) using the 18-kDa translocator protein (TSPO) PET imaging in the hippocampus and precuneus, the 2 AD-vulnerable regions, and to evaluate the association of baseline neuroinflammation with amyloidosis, tau, and longitudinal cognitive decline. METHODS: Twenty-four participants from the Knight Alzheimer Disease Research Center (Knight ADRC) were enrolled and classified into stable cognitively normal, progressor, and symptomatic AD groups based on clinical dementia rating (CDR) at 2 or more clinical assessments. The baseline TSPO radiotracer [11C]PK11195 was used to image microglial activation. Baseline CSF concentrations of Aβ42, Aβ42/Aβ40 ratio, tau phosphorylated at position 181 (p-tau181), and total tau (t-tau) were measured. Clinical and cognitive decline were examined with longitudinal CDR and cognitive composite scores (Global and Knight ADRC-Preclinical Alzheimer Cognitive Composite [Knight ADRC-PACC] Score). RESULTS: Participants in the progressor and symptomatic AD groups had significantly elevated [11C]PK11195 standard uptake value ratios (SUVRs) in the hippocampus but not in the precuneus region. In the subcohort with CSF biomarkers (16 of the 24), significant negative correlations between CSF Aβ42 or Aβ42/Aβ40 and [11C]PK11195 SUVR were observed in the hippocampus and precuneus. No correlations were observed between [11C]PK11195 SUVR and CSF p-tau181 or t-tau at baseline in those regions. Higher baseline [11C]PK11195 SUVR averaged in the whole cortical regions predicted longitudinal decline on cognitive tests. DISCUSSION: Microglial activation is increased in individuals with brain amyloidosis and predicts worsening cognition in AD. CLASSIFICATION OF EVIDENCE: This study provides Class II evidence that in patients with AD, higher baseline [11C]PK11195 SUVR averaged in the whole cortical regions was associated with longitudinal decline on cognitive tests

    Plasma glial fibrillary acidic protein in autosomal dominant Alzheimer\u27s disease: Associations with Aβ-PET, neurodegeneration, and cognition

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    Background: Glial fibrillary acidic protein (GFAP) is a promising candidate blood-based biomarker for Alzheimer\u27s disease (AD) diagnosis and prognostication. The timing of its disease-associated changes, its clinical correlates, and biofluid-type dependency will influence its clinical utility. Methods: We evaluated plasma, serum, and cerebrospinal fluid (CSF) GFAP in families with autosomal dominant AD (ADAD), leveraging the predictable age at symptom onset to determine changes by stage of disease. Results: Plasma GFAP elevations appear a decade before expected symptom onset, after amyloid beta (A ) accumulation and prior to neurodegeneration and cognitive decline. Plasma GFAP distinguished A -positive from A -negative ADAD participants and showed a stronger relationship with A load in asymptomatic than symptomatic ADAD. Higher plasma GFAP was associated with the degree and rate of neurodegeneration and cognitive impairment. Serum GFAP showed similar relationships, but these were less pronounced for CSF GFAP. Conclusion: Our findings support a role for plasma GFAP as a clinical biomarker of A -related astrocyte reactivity that is associated with cognitive decline and neurodegeneration. Highlights: Plasma glial fibrillary acidic protein (GFAP) elevations appear a decade before expected symptom onset in autosomal dominant Alzheimer\u27s disease (ADAD). Plasma GFAP was associated to amyloid positivity in asymptomatic ADAD. Plasma GFAP increased with clinical severity and predicted disease progression. Plasma and serum GFAP carried similar information in ADAD, while cerebrospinal fluid GFAP did not
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