Alexis P. Applequist Data-verified
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Researcher
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Biography and Research Information
OverviewAI-generated summary
Alexis P. Applequist's research investigates the progression of calcific aortic valve disease using a three-dimensional valve-on-chip microphysiological system. This system has implicated cell cycle progression, cholesterol metabolism, and protein homeostasis in the early stages of the disease. Applequist has also developed an in vitro mitral valve model that allows for static trans-mitral pressure studies by utilizing a vacuum to close the valve. Further research includes characterizing piezoelectric-blended polydimethylsiloxane for its potential as a responsive cell culture substrate. Applequist has authored four publications with 22 citations and an h-index of 3. Key collaborators include Kartik Balachandran, Gustavo Vaca-Diez, Ishita Tandon, and Alan E. Woessner, all affiliated with the University of Arkansas at Fayetteville.
Metrics
- h-index: 3
- Publications: 5
- Citations: 25
Selected Publications
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Characterizing Piezoelectric‐Blended Polydimethylsiloxane for Use as a Mechanoelectrical Responsive Cell Culture Substrate (2025)
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A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression (2024)
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In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure (2022)
Collaboration Network
Top Collaborators
- A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression
- Characterizing Piezoelectric‐Blended Polydimethylsiloxane for Use as a Mechanoelectrical Responsive Cell Culture Substrate
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- In Vitro Mitral Valve Model with Unrestricted Ventricular Access: Using Vacuum to Close the Valve and Enable Static Trans-Mitral Pressure
- A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression
- A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression
- A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression
- A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression
- A three-dimensional valve-on-chip microphysiological system implicates cell cycle progression, cholesterol metabolism and protein homeostasis in early calcific aortic valve disease progression
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