Relevant bibliographies by topics / Normobaric oxygen paradox (NOP)

Contents

  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Normobaric oxygen paradox (NOP)'

Author: Grafiati
Published: 16 November 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Normobaric oxygen paradox (NOP).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Normobaric oxygen paradox (NOP)"

1

Lafère, Pierre, Thomas Schubert, David De Bels, Peter Germonpré, and Costantino Balestra. "Can the normobaric oxygen paradox (NOP) increase reticulocyte count after traumatic hip surgery?" Journal of Clinical Anesthesia 25, no. 2 (March 2013): 129–34. http://dx.doi.org/10.1016/j.jclinane.2012.06.021.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Fratantonio, Deborah, Fabio Virgili, Alessandro Zucchi, Kate Lambrechts, Tiziana Latronico, Pierre Lafère, Peter Germonpré, and Costantino Balestra. "Increasing Oxygen Partial Pressures Induce a Distinct Transcriptional Response in Human PBMC: A Pilot Study on the “Normobaric Oxygen Paradox”." International Journal of Molecular Sciences 22, no. 1 (January 5, 2021): 458. http://dx.doi.org/10.3390/ijms22010458.

Full text
Abstract:
The term “normobaric oxygen paradox” (NOP), describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as oxygen shortage, and resulting in up-regulation of the Hypoxia-inducible factor 1α (HIF-1α) transcription factor activity. The molecular characteristics of this response have not been yet fully characterized. Herein, we report the activation time trend of oxygen-sensitive transcription factors in human peripheral blood mononuclear cells (PBMCs) obtained from healthy subjects after one hour of exposure to mild (MH), high (HH) and very high (VHH) hyperoxia, corresponding to 30%, 100%, 140% O2, respectively. Our observations confirm that MH is perceived as a hypoxic stress, characterized by the activation of HIF-1α and Nuclear factor (erythroid-derived 2)-like 2 (NRF2), but not Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB). Conversely, HH is associated to a progressive loss of NOP response and to an increase in oxidative stress leading to NRF2 and NF-kB activation, accompanied by the synthesis of glutathione (GSH). After VHH, HIF-1α activation is totally absent and oxidative stress response, accompanied by NF-κB activation, is prevalent. Intracellular GSH and Matrix metallopeptidase 9 (MMP-9) plasma levels parallel the transcription factors activation pattern and remain elevated throughout the observation time. In conclusion, our study confirms that, in vivo, the return to normoxia after MH is sensed as a hypoxic trigger characterized by HIF-1α activation. On the contrary, HH and VHH induce a shift toward an oxidative stress response, characterized by NRF2 and NF-κB activation in the first 24 h post exposure.
APA, Harvard, Vancouver, ISO, and other styles
3

Balestra, Costantino, Sara Baldelli, Fabio Virgili, Michele Salvagno, Simona Mrakic-Sposta, and Deborah Fratantonio. "Pulsed Hyperoxia Acts on Plasmatic Advanced Glycation End Products and Advanced Oxidation Protein Products and Modulates Mitochondrial Biogenesis in Human Peripheral Blood Mononuclear Cells: A Pilot Study on the “Normobaric Oxygen Paradox”." International Journal of Molecular Sciences 25, no. 4 (February 18, 2024): 2394. http://dx.doi.org/10.3390/ijms25042394.

Full text
Abstract:
The “normobaric oxygen paradox” (NOP) describes the response to the return to normoxia after a hyperoxic event, sensed by tissues as an oxygen shortage, up-regulating redox-sensitive transcription factors. We have previously characterized the time trend of oxygen-sensitive transcription factors in human PBMCs, in which the return to normoxia after 30% oxygen is sensed as a hypoxic trigger, characterized by hypoxia-induced factor (HIF-1) activation. On the contrary, 100% and 140% oxygen induce a shift toward an oxidative stress response, characterized by NRF2 and NF-kB activation in the first 24 h post exposure. Herein, we investigate whether this paradigm triggers Advanced Glycation End products (AGEs) and Advanced Oxidation Protein Products (AOPPs) as circulating biomarkers of oxidative stress. Secondly, we studied if mitochondrial biogenesis was involved to link the cellular response to oxidative stress in human PBMCs. Our results show that AGEs and AOPPs increase in a different manner according to oxygen dose. Mitochondrial levels of peroxiredoxin (PRX3) supported the cellular response to oxidative stress and increased at 24 h after mild hyperoxia, MH (30% O2), and high hyperoxia, HH (100% O2), while during very high hyperoxia, VHH (140% O2), the activation was significantly high only at 3 h after oxygen exposure. Mitochondrial biogenesis was activated through nuclear translocation of PGC-1α in all the experimental conditions. However, the consequent release of nuclear Mitochondrial Transcription Factor A (TFAM) was observed only after MH exposure. Conversely, HH and VHH are associated with a progressive loss of NOP response in the ability to induce TFAM expression despite a nuclear translocation of PGC-1α also occurring in these conditions. This study confirms that pulsed high oxygen treatment elicits specific cellular responses, according to its partial pressure and time of administration, and further emphasizes the importance of targeting the use of oxygen to activate specific effects on the whole organism.
APA, Harvard, Vancouver, ISO, and other styles
4

Balestra, Costantino, Kate Lambrechts, Simona Mrakic-Sposta, Alessandra Vezzoli, Morgan Levenez, Peter Germonpré, Fabio Virgili, Gerardo Bosco, and Pierre Lafère. "Hypoxic and Hyperoxic Breathing as a Complement to Low-Intensity Physical Exercise Programs: A Proof-of-Principle Study." International Journal of Molecular Sciences 22, no. 17 (September 4, 2021): 9600. http://dx.doi.org/10.3390/ijms22179600.

Full text
Abstract:
Inflammation is an adaptive response to both external and internal stimuli including infection, trauma, surgery, ischemia-reperfusion, or malignancy. A number of studies indicate that physical activity is an effective means of reducing acute systemic and low-level inflammation occurring in different pathological conditions and in the recovery phase after disease. As a proof-of-principle, we hypothesized that low-intensity workout performed under modified oxygen supply would elicit a “metabolic exercise” inducing a hormetic response, increasing the metabolic load and oxidative stress with the same overall effect expected after a higher intensity or charge exercise. Herein, we report the effect of a 5-week low-intensity, non-training, exercise program in a group of young healthy subjects in combination with the exposure to hyperoxia (30% and 100% pO2, respectively) or light hypoxia (15% pO2) during workout sessions on several inflammation and oxidative stress parameters, namely hemoglobin (Hb), redox state, nitric oxide metabolite (NOx), inducible nitric oxide synthase (iNOS), inflammatory cytokine expression (TNF-α, interleukin (IL)-6, IL-10), and renal functional biomarkers (creatinine, neopterin, and urates). We confirmed our previous reports demonstrating that intermittent hyperoxia induces the normobaric oxygen paradox (NOP), a response overlapping the exposure to hypoxia. Our data also suggest that the administration of modified air composition is an expedient complement to a light physical exercise program to achieve a significant modulation of inflammatory and immune parameters, including cytokines expression, iNOS activity, and oxidative stress parameters. This strategy can be of pivotal interest in all those conditions characterized by the inability to achieve a sufficient workload intensity, such as severe cardiovascular alterations and articular injuries failing to effectively gain a significant improvement of physical capacity.
APA, Harvard, Vancouver, ISO, and other styles
5

Debevec, Tadej, Michail E. Keramidas, Barbara Norman, Thomas Gustafsson, Ola Eiken, and Igor B. Mekjavic. "No Evidence For The "Normobaric Oxygen Paradox"." Medicine & Science in Sports & Exercise 43, Suppl 1 (May 2011): 151. http://dx.doi.org/10.1249/01.mss.0000403127.23300.30.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Balestra, Costantino, Peter Germonpré, Jacques R. Poortmans, and Alessandro Marroni. "Serum erythropoietin levels in healthy humans after a short period of normobaric and hyperbaric oxygen breathing: the “normobaric oxygen paradox”." Journal of Applied Physiology 100, no. 2 (February 2006): 512–18. http://dx.doi.org/10.1152/japplphysiol.00964.2005.

Full text
Abstract:
Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24–36 h. A 60% increase ( P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the “normobaric oxygen paradox,” does not appear to be present after hyperbaric oxygen breathing.
APA, Harvard, Vancouver, ISO, and other styles
7

Salvagno, Michele, Giacomo Coppalini, Fabio Silvio Taccone, Giacomo Strapazzon, Simona Mrakic-Sposta, Monica Rocco, Maher Khalife, and Costantino Balestra. "The Normobaric Oxygen Paradox—Hyperoxic Hypoxic Paradox: A Novel Expedient Strategy in Hematopoiesis Clinical Issues." International Journal of Molecular Sciences 24, no. 1 (December 21, 2022): 82. http://dx.doi.org/10.3390/ijms24010082.

Full text
Abstract:
Hypoxia, even at non-lethal levels, is one of the most stressful events for all aerobic organisms as it significantly affects a wide spectrum of physiological functions and energy production. Aerobic organisms activate countless molecular responses directed to respond at cellular, tissue, organ, and whole-body levels to cope with oxygen shortage allowing survival, including enhanced neo-angiogenesis and systemic oxygen delivery. The benefits of hypoxia may be evoked without its detrimental consequences by exploiting the so-called normobaric oxygen paradox. The intermittent shift between hyperoxic-normoxic exposure, in addition to being safe and feasible, has been shown to enhance erythropoietin production and raise hemoglobin levels with numerous different potential applications in many fields of therapy as a new strategy for surgical preconditioning aimed at frail patients and prevention of postoperative anemia. This narrative review summarizes the physiological processes behind the proposed normobaric oxygen paradox, focusing on the latest scientific evidence and the potential applications for this strategy. Future possibilities for hyperoxic-normoxic exposure therapy include implementation as a synergistic strategy to improve a patient’s pre-surgical condition, a stimulating treatment in critically ill patients, preconditioning of athletes during physical preparation, and, in combination with surgery and conventional chemotherapy, to improve patients’ outcomes and quality of life.
APA, Harvard, Vancouver, ISO, and other styles
8

Keramidas, Michail E., Ola Eiken, and Igor B. Mekjavic. "Prevailing evidence contradicts the notion of a “normobaric oxygen paradox”." European Journal of Applied Physiology 112, no. 12 (March 31, 2012): 4177–78. http://dx.doi.org/10.1007/s00421-012-2394-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Balestra, C., and P. Germonpré. "Hypoxia, a multifaceted phenomenon: the example of the “Normobaric Oxygen Paradox”." European Journal of Applied Physiology 112, no. 12 (March 31, 2012): 4173–75. http://dx.doi.org/10.1007/s00421-012-2392-y.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Balestra, C., and P. Germonpré. "Increasing EPO using the normobaric oxygen paradox: a ‘not so simple’ task." Acta Physiologica 203, no. 2 (August 31, 2011): 287–88. http://dx.doi.org/10.1111/j.1748-1716.2011.02282.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Normobaric oxygen paradox (NOP)"

1

Leveque, Clément. "Etude des variations de pressions partielles d'oxygène sur les réactions cellulaires chez le sujet sain." Electronic Thesis or Diss., Brest, 2024. http://www.theses.fr/2024BRES0040.

Full text
Abstract:
La compréhension de l'impact de l'oxygène sur les organismes révèle des réponses cellulaires complexes. Des études exposant des sujets sains pendant 1 heure à diverses pressions partielles d'oxygène révèlent des différences quantitatives et cinétiques significatives des réponses cellulaires. En hypoxie normobare, un pic de radicaux libres d’oxygène est observé 30 minutes après l’exposition, sans activation immédiate de réponses antioxydantes. L’interleukine-6 augmente progressivement, atteignant un pic à 8h, reflétant une inflammation évolutive. En hyperoxie normobare, la production de radicaux libres d’oxygène augmente plus tardivement avec une inhibition de l'interleukine 6 observée 2 heures après exposition, suivie d'un pic à 24 heures et un retour à la ligne de base après 48 heures. En hyperoxie hyperbare, une élévation rapide et soutenue des radicaux libres d’oxygène est observée jusqu'à 48 heures, sans distinction significative entre les expositions à 140% et 250% de FiO2. La catalase est rapidement stimulée et maintenue au-delà de 48 heures, démontrant une activation des mécanismes de protection contre l'oxydation. Cette complexité souligne l'importance d'une exploration approfondie des mécanismes cellulaires et de la biogenèse moléculaire intracellulaire, offrant des perspectives prometteuses pour des avancées dans le domaine de la physiologie
Understanding the impact of oxygen on organisms reveals complex cellular responses. Studies exposing healthy subjects during one hour, to various partial pressures of oxygen reveal significant quantitative and kinetic differences in cellular responses. In normobaric hypoxia, a peak of oxygen free radicals is observed 30 minutes after exposure, without immediate activation of antioxidant responses. Interleukin-6 gradually increases, reaching a peak at 8 hours, reflecting evolving inflammation. In normobaric hyperoxia, the production of oxygen free radicals increases later, with inhibition of interleukin-6 observed 2 hours after exposure, followed by a peak at 24 hours and a return to baseline after 48 hours. In hyperbaric hyperoxia, a rapid and sustained elevation of oxygen free radicals is observed for up to 48 hours, with no significant distinction between exposures to 140% and 250% FiO2. Catalase is rapidly stimulated and maintained beyond 48 hours, demonstrating activation of oxidation protection mechanisms. This complexity underscores the importance of thorough exploration of cellular mechanisms and intracellular molecular biogenesis, offering promising perspectives for advances in the field of physiology
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Normobaric oxygen paradox (NOP)' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography