Biography and Research Information
OverviewAI-generated summary
Bhawana Adhikari's research investigates the mechanisms underlying disease development and potential protective strategies. Her work has explored the role of atrogene signaling in preventing musculoskeletal and cardiac issues associated with glucocorticoid use, identifying specific pathways targeted by vitamin D signaling. Adhikari has also contributed to understanding discrepancies in lactate measurement, specifically those caused by beta-hydroxybutyrate interference between different laboratory instruments. This work has implications for accurate clinical diagnostics. Her publications include collaborative efforts with researchers such as Amy Y. Sato, Teresita Bellido, and Hoda A. Hagrass at the University of Arkansas for Medical Sciences.
Metrics
- h-index: 2
- Publications: 7
- Citations: 8
Selected Publications
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A falsely low lactate: discrepancies in lactate measurement between blood gas and core laboratory instruments due to β-hydroxybutyrate interference—a case report (2025)
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A-087 A case study on discrepancies in lactate measurement between blood gas and core laboratory instruments due to beta-hydroxybutyrate interference (2025)
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Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease (2024)
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OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway (2023)
Collaboration Network
Top Collaborators
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway
- A-087 A case study on discrepancies in lactate measurement between blood gas and core laboratory instruments due to beta-hydroxybutyrate interference
- A falsely low lactate: discrepancies in lactate measurement between blood gas and core laboratory instruments due to β-hydroxybutyrate interference—a case report
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- A falsely low lactate: discrepancies in lactate measurement between blood gas and core laboratory instruments due to β-hydroxybutyrate interference—a case report
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