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Alterations in mitochondrial function as a harbinger of cardiomyopathy: Lessons from the dystrophic heart

Journal of molecular and cellular cardiology, 2010-02, Vol.48 (2), p.310-321

2010

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Muscle denervation promotes opening of the permeability transition pore and increases the expression of cyclophilin D

The Journal of physiology, 2006-07, Vol.574 (1), p.319-327

2006

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Early predictors of cardiac decompensation in experimental volume overload

Molecular and cellular biochemistry, 2010-05, Vol.338 (1-2), p.271-282

2010

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Sargramostim (rhu GM-CSF) Improves Survival of Non-Human Primates with Severe Bone Marrow Suppression after Acute, High-Dose, Whole-Body Irradiation

Radiation research, 2021-02, Vol.195 (2), p.191

2021

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Telemetry video-electroencephalography (EEG) in rats, dogs and non-human primates: Methods in follow-up safety pharmacology seizure liability assessments

Journal of pharmacological and toxicological methods, 2014-11, Vol.70 (3), p.230-240

2014

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Characterization of a partial-body irradiation model with oral cavity shielding in nonhuman primates

International journal of radiation biology, 2020-01, Vol.96 (1), p.100-111

2020

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Resistance to Ca2+-induced opening of the permeability transition pore differs in mitochondria from glycolytic and oxidative muscles

American journal of physiology. Regulatory, integrative and comparative physiology, 2008-08, Vol.295 (2), p.R659-R668

2008

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Stress-induced opening of the permeability transition pore in the dystrophin-deficient heart is attenuated by acute treatment with sildenafil

American journal of physiology. Heart and circulatory physiology, 2011-01, Vol.300 (1), p.H144-H153

2011

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Exercise training induces respiratory substrate-specific decrease in Ca2+-induced permeability transition pore opening in heart mitochondria

American journal of physiology. Heart and circulatory physiology, 2006-04, Vol.290 (4), p.H1549-H1557

2006

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Increased expression and intramitochondrial translocation of cyclophilin-D associates with increased vulnerability of the permeability transition pore to stress-induced opening during compensated ventricular hypertrophy

Journal of molecular and cellular cardiology, 2009-03, Vol.46 (3), p.420-430

2009

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Non-invasive measure of respiratory mechanics and conventional respiratory parameters in conscious large animals by high frequency Airwave Oscillometry

Journal of pharmacological and toxicological methods, 2014-07, Vol.70 (1), p.62-65

2014

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Cyclophilin‐D is dispensable for atrophy and mitochondrial apoptotic signalling in denervated muscle

The Journal of physiology, 2011-02, Vol.589 (4), p.855-861

2011

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Compensated volume overload increases the vulnerability of heart mitochondria without affecting their functions in the absence of stress

Journal of molecular and cellular cardiology, 2006-12, Vol.41 (6), p.998-1009

2006

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Short Term Training Attenuates Opening of the Mitochondrial Permeability Transition Pore Without Affecting Myocardial Function Following Ischemia-Reperfusion

Molecular and cellular biochemistry, 2006-10, Vol.291 (1), p.39-47

2006

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Alterations in mitochondrial function as a harbinger of cardiomyopathy: Lessons from the dystrophic heart

Muscle denervation promotes opening of the permeability transition pore and increases the expression of cyclophilin D

Early predictors of cardiac decompensation in experimental volume overload

Sargramostim (rhu GM-CSF) Improves Survival of Non-Human Primates with Severe Bone Marrow Suppression after Acute, High-Dose, Whole-Body Irradiation

Telemetry video-electroencephalography (EEG) in rats, dogs and non-human primates: Methods in follow-up safety pharmacology seizure liability assessments

Characterization of a partial-body irradiation model with oral cavity shielding in nonhuman primates

Resistance to Ca2+-induced opening of the permeability transition pore differs in mitochondria from glycolytic and oxidative muscles

Stress-induced opening of the permeability transition pore in the dystrophin-deficient heart is attenuated by acute treatment with sildenafil

Exercise training induces respiratory substrate-specific decrease in Ca2+-induced permeability transition pore opening in heart mitochondria

Increased expression and intramitochondrial translocation of cyclophilin-D associates with increased vulnerability of the permeability transition pore to stress-induced opening during compensated ventricular hypertrophy

Non-invasive measure of respiratory mechanics and conventional respiratory parameters in conscious large animals by high frequency Airwave Oscillometry

Cyclophilin‐D is dispensable for atrophy and mitochondrial apoptotic signalling in denervated muscle

Compensated volume overload increases the vulnerability of heart mitochondria without affecting their functions in the absence of stress

Short Term Training Attenuates Opening of the Mitochondrial Permeability Transition Pore Without Affecting Myocardial Function Following Ischemia-Reperfusion

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