Academic literature on the topic 'Oroboros Oxygraph-2k'

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Journal articles on the topic "Oroboros Oxygraph-2k"

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Petrus, Alexandra, Corina Ratiu, Lavinia Noveanu, et al. "Assessment of Mitochondrial Respiration in Human Platelets." Revista de Chimie 68, no. 4 (2017): 768–71. http://dx.doi.org/10.37358/rc.17.4.5549.

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It has been long recognized that the impairment of platelet mitochondrial function occurs in a broad spectrum of diseases. Accordingly, the assessment of platelet respiratory dys/function has emerged as a putative approach allowing the characterization of the early impairment of human bioenergetic profile in several chronic pathologies. The aim of this study was to standardize the methodology for platelet isolation from peripheral blood and the measurement of mitochondrial oxygen consumption by means of high-resolution respirometry, respectively. The platelet isolation protocol consisted of tw
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Hoppel, Florian, Luiz Felipe Garcia-Souza, Wilhelm Kantner-Rumplmair, et al. "Human Platelet Mitochondrial Function Reflects Systemic Mitochondrial Alterations: A Protocol for Application in Field Studies." Cells 10, no. 8 (2021): 2088. http://dx.doi.org/10.3390/cells10082088.

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Human blood cells may offer a minimally invasive strategy to study systemic alterations of mitochondrial function. Here we tested the reliability of a protocol designed to study mitochondrial respiratory control in human platelets (PLTs) in field studies, using high-resolution respirometry (HRR). Several factors may trigger PLT aggregation during the assay, altering the homogeneity of the cell suspension and distorting the number of cells added to the two chambers (A, B) of the Oroboros Oxygraph-2k (O2k). Thus, inter-chamber variability (∆ab) was calculated by normalizing oxygen consumption to
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Krylova, T. D., P. G. Tsygankova, Yu S. Itkis, et al. "High resolution respirometry in diagnostic of mitochondrial disorders caused by mitochondrial complex I deficiency." Biomeditsinskaya Khimiya 63, no. 4 (2017): 327–33. http://dx.doi.org/10.18097/pbmc20176304327.

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Complex I (CI) deficiency is one of the most common defects in the OXPHOS system; it represents more than 30% cases of mitochondrial diseases. The group is characterized by clinical and genetic heterogeneity and comprise several nosological forms. The most prevalent phenotypes for CI are LHON and Leigh syndrome. In this study we have analyzed skin fibroblasts from 11 patients with mutations in mtDNA, which cause LHON or Leigh-like phenotypes: m.11778 G>A (n=3), m.3460 A>G (n=2), m.3635 G>A (n=1), m.3308 T>G (n=2), m.3472 T>C (n=1) and 2 patients with earlier unknown substitution
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Burmeister, David M., Belinda Gomez, Tiffany Heard, et al. "9 The Potential for Mitochondrial Respiration and Circulating mtDNA Levels for Early Diagnosis of Sepsis in Burn Patients." Journal of Burn Care & Research 41, Supplement_1 (2020): S9. http://dx.doi.org/10.1093/jbcr/iraa024.013.

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Abstract Introduction Sepsis is a common consequence of burns associated with greater morbidity. While early treatment of sepsis in burn patients improves outcomes identifying sensitive biomarkers has proven difficult. In burns, sepsis often occurs in the absence of positive blood cultures, and associated inflammation precludes the use of inflammatory markers. We hypothesized that lymphocyte mitochondrial bioenergetics and/or circulating mtDNA (a Damage-Associated Molecular Pattern) may serve as novel sepsis biomarkers in burn patients. Methods Whole blood was obtained from adult patients (19–
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Roy Chowdhury, Subir, Saleh Ryan, Cheryl Peltier та ін. "Venetoclax in Combination with NAMPT Inhibitors Decreases Mitochondrial Bioenergetics through the Impaired AMPK/SIRT/PGC1α Signaling Pathway in CLL". Blood 132, Supplement 1 (2018): 1368. http://dx.doi.org/10.1182/blood-2018-99-112210.

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Abstract Objective: Chronic lymphocytic leukemia (CLL) is one of the most common types of leukemia in adults. Altered mitochondrial metabolism has been shown to be involved in the pathogenesis of CLL. Nicotinamidephospho-ribosyltransferase (NAMPT) is a key enzyme in the nicotinamide adenine dinucleotide (NAD) salvage pathway. FK866 and GMX1778, chemical inhibitors of NAMPT, deplete cellular NAD and ATP levels and trigger apoptosis in CLL cells, suggesting NAMPT contributes to the prolonged survival of these cells. Venetoclax is an approved therapy for CLL and blocks the anti-apoptotic B-cell l
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Roy Chowdhury, Subir, Amandeep Singh, Edwin Nguyen та ін. "Ibrutinib in Combination with Venetoclax Decreases Mitochondrial Bioenergetics through the Impaired BTK, AKT and AMPK/SIRT/PGC-1α Signaling Pathway in CLL". Blood 134, Supplement_1 (2019): 1282. http://dx.doi.org/10.1182/blood-2019-127562.

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Objective: Chronic lymphocytic leukemia (CLL) is one of the most common types of leukemia in adults. Altered mitochondrial metabolism has been shown to be involved in the pathogenesis of CLL. Ibrutinib, an inhibitor of Bruton's tyrosine kinase (BTK), and venetoclax, an inhibitor of B-cell lymphoma 2 (Bcl-2) protein are approved therapies for CLL. The adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) signaling axis senses the metabolic demands of cells and regulates mitochondrial function. Silent information regulato
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FERKO, M., I. KANCIROVÁ, M. JAŠOVÁ, et al. "Remote Ischemic Preconditioning of the Heart: Protective Responses in Functional and Biophysical Properties of Cardiac Mitochondria." Physiological Research, December 16, 2014, S469—S478. http://dx.doi.org/10.33549/physiolres.932933.

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Remote ischemic preconditioning (RIP)-induced protection of myocardial energetics was well documented on the level of tissue, but data concerning the involvement of mitochondria were missing. We aimed at the identification of changes in membrane properties and respiratory functions induced in rat heart mitochondria by RIP. Experiments were performed on 46 male Wistar rats divided into control and RIP-treated groups of 21 animals each. Blood flow in the occluded area was recorded by MRI angiography in four animals. RIP protocol comprised of three successive 5-min occlusions each followed by 5-m
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Tomar, Namrata, Sunil M. Kandel, Xiao Zhang, Nadezhda Zheleznova, Allen W. Cowley, and Ranjan K. Dash. "Abstract 16: Progressive Alterations Of Mitochondrial Bioenergetics In The Kidney During The Development Of Salt-induced Hypertension." Hypertension 76, Suppl_1 (2020). http://dx.doi.org/10.1161/hyp.76.suppl_1.16.

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Hypertension is a complex disease and a leading cause of morbidity and mortality globally. Although oxidative stress and mitochondrial dysfunction have been found in the kidney in various models of hypertension, progressive alteration of mitochondrial oxidative phosphorylation (OxPhos) in the kidney during the development of salt-sensitive hypertension has not been characterized. The present study determined changes of OxPhos in kidneys of Dahl salt-sensitive (SS) rats before (0.4% NaCl diet; LS) and after switching to a high salt diet (4.0% NaCl; HS) during the development of hypertension. Mi
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Borger, J., D. Scheiber, P. Horn, et al. "Aetiology-dependent impairment of mitochondrial function in the failing human heart." European Heart Journal 41, Supplement_2 (2020). http://dx.doi.org/10.1093/ehjci/ehaa946.3606.

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Abstract Background Alterations of mitochondrial function have been identified to play a role in Heart Failure (HF) pathophysiology. Oxidative phosphorylation (OXPHOS) capacity of the myocardium was shown to be reduced in the failing heart. Ineffective mitochondrial function promotes formation of reactive oxygen species (ROS) that may affect remodelling in ischemia. Thus far, human mitochondrial function comparing dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM) resembling the main aetiologies of heart failure with reduced ejection fraction (HFrEF) has not been investigated. Purp
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Zhang, Xiaolei, and Coen Paul. "PO-264 Target Mitochondria Metabolism and Energy Expenditure in Muscle Atrophy, Sarcopenia and Cachexia." Exercise Biochemistry Review 1, no. 5 (2018). http://dx.doi.org/10.14428/ebr.v1i5.11123.

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Objective Muscle atrophy is a common and clinically important outcome of many diseases and hospitalization bed rest. Mechanical unloading of skeletal muscles may result in a rapid loss of muscle mass and mitochondria dysfunction. And the recovery from disuse muscle atrophy is usually complete in young healthy adults but is delayed and often incomplete in older patients. However, the mechanisms underlying poor recovery of aged muscle following disuse remain to be delineated. Recent evidence suggests that mitochondrial energetics play an important role in regulation of muscle mass. To this end,
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Dissertations / Theses on the topic "Oroboros Oxygraph-2k"

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Cadonic, Chris. "Modelling mitochondrial complex IV bioenergetics." 2016. http://hdl.handle.net/1993/31602.

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A computational model for mitochondrial function has been developed from oxygen concentration data measured in the Oroboros Oxygraph-2k and oxygen consumption rates measured in the Seahorse XF24 Analyzer. Measurements were acquired using embryonic-cultured cortical neurons and isolated mitochondria from CD1 mice. Based on the biological mechanism of mitochondrial activity, a computational model was developed using biochemical kinetic modelling. To modulate mitochondrial activity, dysfunctions were introduced by injecting the inhibiting reagents oligomycin, rotenone, and antimycin A, and the un
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Book chapters on the topic "Oroboros Oxygraph-2k"

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Long, Qinqiang, Lizhen Huang, Kai Huang, and Qinglin Yang. "Assessing Mitochondrial Bioenergetics in Isolated Mitochondria from Mouse Heart Tissues Using Oroboros 2k-Oxygraph." In Methods in Molecular Biology. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9195-2_19.

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Hall, Arnaldur, and S. Moein Moghimi. "Determination of Polycation-Mediated Perturbation of Mitochondrial Respiration in Intact Cells by High-Resolution Respirometry (Oxygraph-2k, OROBOROS)." In Nanotechnology for Nucleic Acid Delivery. Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9092-4_20.

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