Assessment of Mitochondrial Metabolic Oxidative State in Living Cardiomyocytes with Cardiomyocyte Autofluorescence
Bibliographic record
Abstract
Objective: To study fingerprinting of mitochondrial metabolic oxidative state in living cardiomyocytes with cadiomyocyte autofluorescence(AF) in order to monitor cellular fluorescence of nicotinamide adenine dinucleotide(phosphate)[NAD(P)H],the principal electron donor in mitochondrial respiration which is responsible for vital ATP supply to sensitively and reflects early signs of mitochondrial function in pathophysiological conditions,such as ischemia,diabetes and heart failure.Methods: NAD(P)H was studied as a marker for non-invasive fluorescent probing of the mitochondrial function.NAD(P)H fluorescence was recorded in living cardiomyocytes following excitation with 375 nm UV-light and detection by spectrally-resolved time-correlated single photon counting(TCSPC),based on the simultaneous measurement of the fluorescence spectra and fluorescence lifetimes.Modulation of mitochondrial respiration was tested by studying dynamic characteristics of NAD(P)H fluorescence decay in living cardiomyocytes.Results: At least a 3-exponential decay model,with 0.4-0.7 ns,1.2-1.9 ns and 8.0-13.0 ns lifetime pools was necessary to describe cardiomyocyte AF within 420-560 nm spectral range.Rotenone,the inhibitor of Complex Ⅰ of the mitochondrial respiratory chain,increased AF intensity and shortened the average fluorescence lifetime.Dinitrophenol(DNP),an uncoupling agent of the mitochondrial oxidative phosphorylation,lowered AF intensity,broadened the spectral shoulder at 520 nm and increased the average fluorescence lifetime.These effects were comparable to the changes in the concentration and in the rate of dehydrogenation of NADH in vitro.Conclusion: Spectrally-resolved fluorescence lifetime technique provides promising new tool for analysis of mitochondrial NAD(P)H fluorescence with good reproducibility in living cardiomyocytes.This approach will enhance our knowledge about cardiomyocyte oxidative metabolism and/or its dysfunction at a cellular level.In the future,this approach can prove helpful in the clinical diagnosis and treatment of mitochondrial disorder.
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How this classification was reachedexpand
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 0.000 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".