Publications by authors named "Rachel L Padget"

Article Synopsis
  • Viral cardiac infections, particularly myocarditis caused by adenovirus, present significant challenges due to the lack of understanding of how these infections lead to sudden cardiac issues, especially in young adults.
  • The study utilizes mouse adenovirus type-3 to model acute cardiac infections, revealing that infection leads to decreased conduction velocity and altered gap junction function before major immune responses occur.
  • Findings indicate that both mouse and human adenoviruses affect cardiac function by increasing Cx43 phosphorylation, which impacts action potential duration and cell synchrony, suggesting a need for further exploration of these mechanisms in both species.
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Background: Folate is an essential B-group vitamin and a key methyl donor with important biological functions including DNA methylation regulation. Normal neurodevelopment and physiology are sensitive to the cellular folate levels. Either deficiency or excess of folate may lead to neurological disorders.

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Recent studies revealed that relatively small changes in perfusate sodium ([Na]) composition significantly affect cardiac electrical conduction and stability in contraction arrested ex vivo Langendorff heart preparations before and during simulated ischemia. Additionally, [Na] modulates cardiomyocyte contractility via a sodium-calcium exchanger (NCX) mediated pathway. It remains unknown, however, whether modest changes to [Na] that promote electrophysiologic stability similarly improve mechanical function during baseline and ischemia-reperfusion conditions.

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Adenoviruses are responsible for a spectrum of pathogenesis including viral myocarditis. The gap junction protein connexin43 (Cx43, gene name GJA1) facilitates rapid propagation of action potentials necessary for each heartbeat. Gap junctions also propagate innate and adaptive antiviral immune responses, but how viruses may target these structures is not understood.

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Blood vessel maturation, which is characterized by the investment of vascular smooth muscle cells (vSMCs) around developing blood vessels, begins when vessels remodel into a hierarchy of proximal arteries and proximal veins that branch into smaller distal capillaries. The ultimate result of maturation is formation of the tunica media-the middlemost layer of a vessel that is composed of vSMCs and acts to control vessel integrity and vascular tone. Though many studies have implicated the role of various signaling molecules in regulating maturation, no studies have determined a role for hemodynamic force in the regulation of maturation in the mouse.

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