Maxine Cooper
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Maxine Cooper has a total of 15 co-authors. Here are the top co-authors by number of shared publications:
- Christine Keven
Liggins Institute, University of Auckland, Auckland 1010, New Zealand
1 shared publication - Edmond Zhang
Precision Driven Health Initiative, Auckland 1021, New Zealand
1 shared publication - Eric Bruce Thorstensen
Liggins Institute, University of Auckland, Auckland 1010, New Zealand
1 shared publication - Erica Zarate
School of Biological Sciences, University of Auckland, Auckland 1010, New Zealand
1 shared publication - Kevin Smith
Clinical Laboratory, Waitemata District Health Board, Auckland 0622, New Zealand
1 shared publication - Margaret Coe
The Liggins Institute, The University of Auckland, Private Bag 92019, Auckland, 1142, New Zealand
1 shared publication
Latest Publications
- Open Access
- 21 December 2022
- Published by MDPI AG in Biomolecules
- Vol. 13 (1) , 13
Metabolomics and a Breath Sensor Identify Acetone as a Biomarker for Heart Failure
Background: Multi-omics delivers more biological insight than targeted investigations. We applied multi-omics to patients with heart failure with reduced ejection fraction (HFrEF). Methods: 46 patients with HFrEF and 20 controls underwent metabolomic profiling, including liquid/gas chromatography mass spectrometry (LC-MS/GC-MS) and solid-phase microextraction (SPME) volatilomics in plasma and urine. HFrEF was defined using left ventricular global longitudinal strain, ejection fraction and NTproBNP. A consumer breath acetone (BrACE) sensor validated results in n = 73. Results: 28 metabolites were identified by GCMS, 35 by LCMS and 4 volatiles by SPME in plasma and urine. Alanine, aspartate and glutamate, citric acid cycle, arginine biosynthesis, glyoxylate and dicarboxylate metabolism were altered in HFrEF. Plasma acetone correlated with NT-proBNP (r = 0.59, 95% CI 0.4 to 0.7), 2-oxovaleric and cis-aconitic acid, involved with ketone metabolism and mitochondrial energetics. BrACE > 1.5 ppm discriminated HF from other cardiac pathology (AUC 0.8, 95% CI 0.61 to 0.92, p < 0.0001). Conclusion: Breath acetone discriminated HFrEF from other cardiac pathology using a consumer sensor, but was not cardiac specific.
- 21 December 2022
- Published by MDPI AG in Biomolecules
- Vol. 13 (1) , 13
Open AccessMetabolomics and a Breath Sensor Identify Acetone as a Biomarker for Heart Failure
Background: Multi-omics delivers more biological insight than targeted investigations. We applied multi-omics to patients with heart failure with reduced ejection fraction (HFrEF). Methods: 46 patients with HFrEF and 20 controls underwent metabolomic profiling, including liquid/gas chromatography mass spectrometry (LC-MS/GC-MS) and solid-phase microextraction (SPME) volatilomics in plasma and urine. HFrEF was defined using left ventricular global longitudinal strain, ejection fraction and NTproBNP. A consumer breath acetone (BrACE) sensor validated results in n = 73. Results: 28 metabolites were identified by GCMS, 35 by LCMS and 4 volatiles by SPME in plasma and urine. Alanine, aspartate and glutamate, citric acid cycle, arginine biosynthesis, glyoxylate and dicarboxylate metabolism were altered in HFrEF. Plasma acetone correlated with NT-proBNP (r = 0.59, 95% CI 0.4 to 0.7), 2-oxovaleric and cis-aconitic acid, involved with ketone metabolism and mitochondrial energetics. BrACE > 1.5 ppm discriminated HF from other cardiac pathology (AUC 0.8, 95% CI 0.61 to 0.92, p < 0.0001). Conclusion: Breath acetone discriminated HFrEF from other cardiac pathology using a consumer sensor, but was not cardiac specific.