Publications by authors named "Katie Hood"

Article Synopsis
  • The study investigates the interaction between Ang-(1-7) and the ET-1 system in the context of pulmonary hypertension, suggesting that Ang-(1-7) opposes harmful effects of ET-1.
  • Research methods include various models (in vivo in mice, ex vivo in isolated arteries, and in vitro in human cells) that demonstrate Ang-(1-7) treatment reduces pulmonary vascular damage and promotes vasodilation.
  • Findings reveal a complex signaling network involving MasR and ETR that protects against vascular injury, highlighting the potential for enhancing this pathway to improve vascular health.
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Purpose: This evaluation describes efforts taken by MIECHV administrators and staff during the pandemic using data collected from 60 MIECHV staff surveys and nine statewide weekly focus groups.

Description: The Florida Maternal, Infant and Early Childhood Home Visiting (MIECHV) Initiative funds perinatal home visiting for pregnant women and families with infants throughout the state. Florida MIECHV has shown resilience to disasters and times of crises in the past, while generating a culture of adaptation and continuous quality improvement among local implementing agencies.

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Aims: We questioned whether aldosterone and oxidative stress play a role in vascular damage in severe hypertension and investigated the role of Nox1 in this process.

Materials And Methods: We studied mesenteric arteries, aortas and vascular smooth muscle cells (VSMC) from WKY and SHRSP rats. Vascular effects of eplerenone or canrenoic acid (CA) (mineralocorticoid receptor (MR) blockers), ML171 (Nox1 inhibitor) and EHT1864 (Rac1/2 inhibitor) were assessed.

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Objective: Serotonin can induce human pulmonary artery smooth muscle cell (hPASMC) proliferation through reactive oxygen species (ROS), influencing the development of pulmonary arterial hypertension (PAH). We hypothesize that in PASMCs, serotonin induces oxidative stress through NADPH-oxidase-derived ROS generation and reduced Nrf-2 (nuclear factor [erythroid-derived 2]-like 2) antioxidant systems, promoting vascular injury.

Approach And Results: HPASMCs from controls and PAH patients, and PASMCs from Nox1 mice, were stimulated with serotonin in the absence/presence of inhibitors of Src kinase, the 5-HT receptor, and NADPH oxidase 1 (Nox1).

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Estrogen and oxidative stress have been implicated in pulmonary arterial hypertension (PAH). Mechanisms linking these systems are elusive. We hypothesized that estrogen metabolite, 16α-hydroxyestrone (16αOHE1), stimulates nicotinamide adenine dinucleotide phosphate oxidase (Nox)-induced reactive oxygen species (ROS) generation and proliferative responses in human pulmonary artery smooth muscle cells (hPASMCs) and that in PAH aberrant growth signaling promotes vascular remodeling.

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Pulmonary arterial hypertension (PAH) is a devastating vasculopathy that predominates in women and has been associated with dysregulated estrogen and serotonin signaling. Overexpression of the serotonin transporter (SERT(+)) in mice results in an estrogen-dependent development of pulmonary hypertension (PH). Estrogen metabolism by cytochrome P450 1B1 (CYP1B1) contributes to the pathogenesis of PAH, and serotonin can increase CYP1B1 expression in human pulmonary arterial smooth muscle cells (hPASMCs).

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A method for making aerogel doped with gold nanoparticles (GNPs) produces a composite material with a well-defined localized surface plasmon resonance peak at 520 nm. The width of the extinction feature indicates the GNPs are well dispersed in the aerogel, making it suited to optical study. A simple effective medium approximation cannot explain the peak extinction wavelengths.

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