Publications by authors named "M Pryor"

Acute Kidney Injury (AKI) is characterized by an abrupt decline in kidney function and has been associated with excess risks of death, kidney disease progression, and cardiovascular events. The kidney has a high energetic demand with mitochondrial health being essential to renal function and damaged mitochondria has been reported across AKI subtypes. 5' adenosine monophosphate-activated protein kinase (AMPK) activation preserves cellular energetics through improvement of mitochondrial function and biogenesis when ATP levels are low such as under ischemia-induced AKI.

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As variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continue to emerge, assessment of vaccine immunogenicity remains a critical factor to support continued vaccination. To this end, an in vitro microneutralization (MN50) assay was validated to quantitate SARS-CoV-2 neutralizing antibodies against prototype and variant strains (Beta, Delta, Omicron BA.1, Omicron BA.

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The Massachusetts Bays National Estuary Partnership is one of 28 programs in the United States Environmental Protection Agency's National Estuary Program (NEP) charged with developing and implementing comprehensive plans for protecting and restoring the biological integrity and beneficial uses of their estuarine systems. The Partnership has recently updated their comprehensive management plan to include restoration targets for coastal habitats, and as part of this effort, the program explored how to better demonstrate that recovery of ecological integrity of degraded ecosystems also provides ecosystem services that humans want and need. An essential step was to identify key stakeholders and understand the benefits important to them.

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Resistance to apoptosis in acute myeloid leukemia (AML) cells causes refractory or relapsed disease, associated with dismal clinical outcomes. Ferroptosis, a mode of non-apoptotic cell death triggered by iron-dependent lipid peroxidation, has been investigated as potential therapeutic modality against therapy-resistant cancers, but our knowledge of its role in AML is limited. We investigated ferroptosis in AML cells and identified its mitochondrial regulation as a therapeutic vulnerability.

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