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Relevant bibliographies by topics / Hyperoxie

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Academic literature on the topic 'Hyperoxie'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 March 2025

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Journal articles on the topic "Hyperoxie"

1

Demiselle, Julien, Peter Radermacher, and Pierre Asfar. "Hyperoxie en réanimation." Anesthésie & Réanimation 5, no. 2 (March 2019): 91–97. http://dx.doi.org/10.1016/j.anrea.2018.12.003.

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Payen, Didier. "Hyperoxie : un réel enjeu ?" Anesthésie & Réanimation 4, no. 2 (March 2018): 134–37. http://dx.doi.org/10.1016/j.anrea.2017.12.011.

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Grafen, Keren. "Wenn die Luft in den Zellen dünn wird." Deutsche Heilpraktiker-Zeitschrift 16, no. 06 (June 2021): 48–52. http://dx.doi.org/10.1055/a-1523-9205.

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SummaryBei einem Sauerstoffmangel setzt der Organismus einen Mechanismus in Gang, der unter anderem durch Anpassung der Energiegewinnung für ein möglichst langes Überleben sorgen soll. Die Intervall-Hypoxie-Hyperoxie-Therapie (IHHT) setzt Hypoxie in Intervallen gezielt ein, um insbesondere Prozesse der verbesserten Energiegewinnung anzuregen, wodurch wiederum Beschwerden reduziert werden sollen. Die Intervall-Hypoxie-Hyperoxie-Therapie (IHHT) kann zum einen bei Beschwerden wie Fatigue helfen, zum anderen aber auch als Höhentraining vor Aufenthalten in hohen Bergen dienen.

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Francony, G., P. Bouzat, J. Picard, M. C. Fevre, S. Gay, and J. F. Payen. "Hyperoxie normobarique chez le patient traumatisé crânien." Annales Françaises d'Anesthésie et de Réanimation 31, no. 3 (March 2012): 224–27. http://dx.doi.org/10.1016/j.annfar.2011.11.009.

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Berger, Marc, Franziska Macholz, Peter Schmidt, and Ragnar Huhn. "Hyperoxie in Anästhesie und Intensivmedizin – Zu viel des Guten?" AINS - Anästhesiologie · Intensivmedizin · Notfallmedizin · Schmerztherapie 51, no. 06 (June 30, 2016): 372–77. http://dx.doi.org/10.1055/s-0041-105156.

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Schmidt, S., W. Decleer, S. Gorissen-Bosselmann, H. Eilers, K. Pringle, N. Helledie, P. Rolfe, and D. Krebs. "Laserspektroskopische Erfassung der induzierten Hyperoxie – eine tierexperimentelle Studie beim Lamm - Laser-spectroscopy of Induced Hyperoxia – An Experimental Study in the Lamb." Biomedizinische Technik/Biomedical Engineering 35, no. 9 (1990): 185–89. http://dx.doi.org/10.1515/bmte.1990.35.9.185.

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Sadek, A., R. Khattab, A. Amer, and A. Youssef. "Protective role of caffeine versus N-acetylcysteine in hyperoxic acute lung injury in neonatal rats." Journal of Morphological Sciences 34, no. 02 (April 2017): 058–67. http://dx.doi.org/10.4322/jms.113617.

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Abstract Introduction: Prolonged breathing of high oxygen concentration leads to hyperoxic acute lung injury. Neonatal Respiratory diseases usually require increased supplement of high oxygen concentrations, so neonates are more susceptible to hyperoxic acute lung injury. The aim of this work was to investigate the protective role of caffeine versus N-acetylcysteine against hyperoxic acute lung injury in neonatal rats. Materials and Methods: 32 albino rats aged seven days were used in this experiment. The pups were divided into four groups; 1) Control or normoxic group; rats placed in normoxic chamber where fraction of inspired oxygen (FiO2) was 0.21, 2) Hyperoxic group; rats were placed in hyperoxic chamber (FiO2>0.8) using an oxygen flow of 1.5 Litre/min, 3) Hyperoxia-CAF group; rats exposed to hyperoxia and received a single intra-peritoneal injection of 20 mg/kg caffeine just prior to exposure, and 4) Hyperoxia-NAC group; rats exposed to hyperoxia and received a single intra-peritoneal injection of 150 mg/kg N-acetylcysteine just prior to exposure. 48 hours after exposure, lung specimens were processed for histological and immunohistochemical study using caspase-3, cluster of differentiation-68-antibody (CD68) and interleukin-1-beta (IL-1β). Results: Neonatal hyperoxia led to severe impairment in lung architecture, with a highly significant increase in alveolar macrophages. Also, caspase and IL-1β immune-reaction were increased significantly as compared to control group. Caffeine could improve the histolopathological picture of hyperoxic acute lung injury, and also could decrease alveolar macrophage count and IL-1β immune-reaction better than N-acetylcysteine. Conclusion: Caffeine is more effective than N-acetylcysteine in prophylaxis against hyperoxic acute lung injury in neonates.

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Xu, Dong, Jill R. Guthrie, Sherry Mabry, Thomas M. Sack, and William E. Truog. "Mitochondrial aldehyde dehydrogenase attenuates hyperoxia-induced cell death through activation of ERK/MAPK and PI3K-Akt pathways in lung epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 5 (November 2006): L966—L975. http://dx.doi.org/10.1152/ajplung.00045.2006.

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Oxygen toxicity is one of the major risk factors in the development of the chronic lung disease or bronchopulmonary dysplasia in premature infants. Using proteomic analysis, we discovered that mitochondrial aldehyde dehydrogenase (mtALDH or ALDH2) was downregulated in neonatal rat lung after hyperoxic exposure. To study the role of mtALDH in hyperoxic lung injury, we overexpressed mtALDH in human lung epithelial cells (A549) and found that mtALDH significantly reduced hyperoxia-induced cell death. Compared with control cells (Neo-A549), the necrotic cell death in mtALDH-overexpressing cells (mtALDH-A549) decreased from 25.3 to 6.5%, 50.5 to 9.1%, and 52.4 to 15.1% after 24-, 48-, and 72-h hyperoxic exposure, respectively. The levels of intracellular and mitochondria-derived reactive oxygen species (ROS) in mtALDH-A549 cells after hyperoxic exposure were significantly lowered compared with Neo-A549 cells. mtALDH overexpression significantly stimulated extracellular signal-regulated kinase (ERK) phosphorylation under normoxic and hyperoxic conditions. Inhibition of ERK phosphorylation partially eliminated the protective effect of mtALDH in hyperoxia-induced cell death, suggesting ERK activation by mtALDH conferred cellular resistance to hyperoxia. mtALDH overexpression augmented Akt phosphorylation and maintained the total Akt level in mtALDH-A549 cells under normoxic and hyperoxic conditions. Inhibition of phosphatidylinositol 3-kinase (PI3K) activation by LY294002 in mtALDH-A549 cells significantly increased necrotic cell death after hyperoxic exposure, indicating that PI3K-Akt activation by mtALDH played an important role in cell survival after hyperoxia. Taken together, these data demonstrate that mtALDH overexpression attenuates hyperoxia-induced cell death in lung epithelial cells through reduction of ROS, activation of ERK/MAPK, and PI3K-Akt cell survival signaling pathways.

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Pournaras, C., K. Strommer, C. Riva, M. Tsacopoulos, and N. Gilodi. "Gradients d'O2dans la rétine du porc-miniature en normoxie et hyperoxie." Klinische Monatsblätter für Augenheilkunde 190, no. 04 (April 1987): 383–84. http://dx.doi.org/10.1055/s-2008-1050418.

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Yao, Qin, Musa A. Haxhiu, Syed I. Zaidi, Shijian Liu, Anjum Jafri, and Richard J. Martin. "Hyperoxia enhances brain-derived neurotrophic factor and tyrosine kinase B receptor expression in peribronchial smooth muscle of neonatal rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 2 (August 2005): L307—L314. http://dx.doi.org/10.1152/ajplung.00030.2005.

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Airway hyperreactivity is one of the hallmarks of hyperoxic lung injury in early life. As neurotrophins such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are potent mediators of neuronal plasticity, we hypothesized that neurotrophin levels in the pulmonary system may be disturbed by hyperoxic exposure. We therefore evaluated the effects of hyperoxia on the expression of BDNF, NGF, and their corresponding high-affinity receptors, TrkB and TrkA, respectively, in the lung of rat pups. Five-day-old Sprague-Dawley rat pups were randomized to hyperoxic or control groups and then continuously exposed to hyperoxia (>95% oxygen) or normoxia over 7 days. At both mRNA and protein levels, BDNF was detected in lung but not in trachea; its level was substantially enhanced in lungs from the hyperoxia-exposed rat pups. Distribution of BDNF mRNA by in situ hybridization indicates that peribronchial smooth muscle was the major source of increased BDNF production in response to hyperoxic exposure. Interestingly, hyperoxia-induced elevation of BDNF was not accompanied by any changes of NGF levels in lung. Furthermore, hyperoxic exposure increased the expression of TrkB in peribronchial smooth muscle but had no effect on the distribution of the specific NGF receptor TrkA. These findings indicate that hyperoxic stress not only upregulates BDNF at mRNA and protein levels but also enhances TrkB within peribronchial smooth muscle. However, there was no corresponding effect on NGF and TrkA receptors. We speculate that the increased level of BDNF may contribute to hyperoxia-induced airway hyperresponsiveness in early postnatal life.

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Dissertations / Theses on the topic "Hyperoxie"

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Höhn, Thomas. "Effekte von Hyperoxie und Stickstoffmonoxid beim Neugeborenen." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965683826.

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Höhn, Thomas. "Effekte von Hyperoxie und Stickstoffmonoxid beim Neugeborenen." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2002. http://dx.doi.org/10.18452/13827.

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In der vorliegenden Arbeit sind Untersuchungen vorgestellt, die sich mit Wirkungen und Interaktionen von zwei ubiquitär im menschlichen Körper vorkommenden Gasen befassen, i.e. Sauerstoff und Stickstoffmonoxid. Im Falle beider Substanzen ermöglicht die geringe Größe der Moleküle eine freie Diffusion über Membranen hinweg, eine Eigenschaft, die für die Funktion der Signaltransduktion geradezu prädestiniert. Aus den vorgelegten Untersuchungen lassen sich die folgenden Folgerungen ableiten: * Stickstoffmonoxid wirkt in-vitro selektiv bakteriostatisch auf Bakterien, die üblicherweise Früh- und Neugeborene besiedeln. Dabei hängt die Selektivität von den jeweiligen bakteriellen Verteidigungsmechanismen ab, die bakteriostatische Wirkung liegt in einem Konzentrationsbereich, der außerhalb desjenigen liegt, der derzeit klinisch angewendet wird. * Hyperoxie führt im Ganztiermodell der unreifen Ratte zu einer zerebralen Hochregulation von iNOS und damit zur Synthese von NO. Soweit dies anhand der Synthese von Peroxynitrit als definitivem Schädigungsmechanismus beurteilbar ist, wird trotz entsprechender iNOS-Expression wenig bis gar kein Peroxynitrit gebildet. Da das Zusammentreffen von NO und Sauerstoff sonst regelhaft zur Entstehung von Peroxynitrit führt, müssen im Gehirn der unreifen Ratte ausreichende antioxidative Schutzmechanismen präsent sein, die diese Reaktion verhindern. * Im in-vitro-Modell der Gasäquilibrierung von Nabelschnur-PMN zeigte sich unter Hyperoxie das ausgeprägteste Aktivierungsmuster aller verglichenen Sauerstoffkonzentrationen. Dies stand im Gegensatz zur Exposition adulter Zellen, hier fand sich eine größere Hyperoxietoleranz bei gleichzeitig stärkster Aktivierung unter Hypoxiebedingungen. Welche Bedeutung diesen Ergebnissen im klinischen Umgang mit Neugeborenen zukommt muß derzeit noch offen bleiben. Allerdings häufen sich Hinweise aus experimentellen Studien, die darauf hindeuten, daß ein restriktiver Umgang mit hohen Sauerstoffkonzentrationen auch im klinischen Umfeld gerechtfertigt sein könnte.
The present investigations deal with the effects and interactions of gases, which are ubiquitous in the human body i.e. oxygen and nitric oxide. Both substances are small enough to freely diffuse across biological membranes. This ability predestines both molecules for the function of signal transduction. The results of our investigations lead to conclusions as follows: * Nitric oxide has selective bacteriostatic effects in-vitro on some bacterial strains typically isolated from preterm and term newborn infants. Selectivity depends on the presence of bacterial defense mechanisms. The bacteriostatic effect takes place at concentrations above those currently used in clinical practice. * Hyperoxia leads to upregulation of iNOS and subsequent NO production in an animal model of the immature rat. Despite this upregulation of iNOS synthesis there is no increased production of peroxynitrite which is known to cause cellular and DNA damage. Since the combination of NO and high concentrations of oxygen lead to peroxynitrite formation on a regular basis, effective antioxidant mechanisms appear to prevent peroxynitrite formation in the brain of the immature rat. * The most pronounced activation of cord blood polymorphonuclear cells (PMN) during conditions of hyperoxia, normoxia, and hypoxia was found for exposure towards high oxygen concentrations in an in-vitro model of gas equilibration. As opposed to that, hypoxia was the most potent trigger for adult PMN. It remains to be determined which clinical implications must be derived from these results. However, increasing experimental evidence indicates that exposure towards high oxygen concentrations should be restricted also in clinical practice and not only in preterm infants, but also in term newborns.

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Endesfelder, Stefanie [Verfasser]. "Protektive Strategien im Hyperoxie-Schädigungsmodell der neonatalen Ratte / Stefanie Endesfelder." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1196803048/34.

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Torrentino-Madamet, Marylin. "Influence des conditions environnementales sur le métabolisme de Plasmodium falciparum." Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX20700/document.

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P. falciparum est le principal responsable des formes graves du paludisme. Le parasiteévolue entre deux hôtes (homme et moustique) qui lui imposent différents environnements; ettout particulièrement, des modifications des pressions partielles d’O2 nécessitant des capacitésd’adaptation surprenantes pour un parasite microaérophile. Chez l’hôte vertébré, lesphénomènes de cytoadhésion, ralentissant la progression du parasite notamment au niveau despoumons, augmentent la durée d’exposition aux conditions hyperoxiques.La dynamique de la réponse parasitaire à l’hyperoxie a été étudiée par une approchecombinée de transcriptomique et de protéomique. Certains mécanismes de défense contre lesespèces réactives d’oxygène ont été appréciés, dont une éventuelle fonction oxydasealternative.L’exposition du parasite à 21% d’O2 induit un retard de croissance au niveau de laschizogonie. Le stress oxydatif induit par l’hyperoxie entraîne des perturbations métaboliquescomme une inhibition de la glycolyse en faveur de la respiration et un ralentissement dumétabolisme de la vacuole digestive. Cette action combinée sur le métabolisme mitochondrialet vacuolaire permet au parasite de s’adapter à un environnement hyperoxydant, en régulant laproduction d’espèces réactives d’oxygène. Nos travaux ont montré qu’un inhibiteur de lafonction oxydase alternative, l’acide salicylhydroxamique ou SHAM, avec un effet mineur surla croissance parasitaire en microaérophilie, avait un effet létal sur les parasites en hyperoxie.Une meilleure compréhension de la biologie parasitaire pourrait contribuer audéveloppement de nouveaux traitements antipaludiques associés à une thérapie hyperbarique
P. falciparum is the main species responsible for severe case of malaria. The parasiteevolves between two hosts (human and mosquito), imposing to it different environments;especially changes in the O2 pressure, demanding astonishing adaptation skills for amicroaerophilic parasite. In the vertebrate host, the phenomena of cytoadhesion, which slowdown the spread of the parasite among others in the lungs, increase the timing of exposure tohyperoxic conditions.The parasitic response dynamic to hyperoxia has been analysed by a combinedtranscriptomic and proteomic approach. Some of the defense mechanisms against reactiveoxygen species have been evaluated, among which a potential alternative oxidase function.The exposure of the parasite to 21%O2 atmosphere leads to a growth delay atschizogony level. The oxidative stress resulting from the hyperoxia conducts to metabolicalterations, as an inhibition of the glycolysis in favour of respiration and as a slowdown of themetabolism of the digestive vacuole. This combined action on the mitochondrial and vacuolarmetabolisms allows the parasite to adapt itself to hyperoxic environment, by regulatingreactive oxygen species. Our works have shown that an inhibitor of the alternative oxidasefunction, the salicylhydroxamic acid or SHAM, with a minor effect on the parasite growth inmicroaerophily, had letal effect on parasites in hyperoxia.A better understanding of the parasitic biology could contribute to the development ofnew antimalarial treatments, associated with a hyperbaric oxygen therapy

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Huyard, Fanny. "Impact du stress hyperoxique en période néonatale sur la structure vasculaire : implication des phénomènes de sénescence et rôle possible dans la programmation développementale de l'hypertension artérielle." Thèse, Université de Lorraine, 2013. http://hdl.handle.net/1866/12773.

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Réalisé en cotutelle avec l'Université de Lorraine (France)
Ce projet traite de la programmation développementale de l’hypertension artérielle (HTA) à travers des influences néonatales précoces pouvant moduler le développement vasculaire. Les bébés prématurés présentent des défenses antioxydantes diminuées comparés aux nouveau-nés à terme et sont exposés à la naissance à des concentrations élevées en oxygène (O2) engendrant la production d’espèces réactives de l’O2 (ERO). Les conséquences vasculaires à long terme de dommages liés aux ERO en période néonatale et les mécanismes impliqués sont très partiellement compris. Les précédents résultats du laboratoire ont montré qu’un stress hyperoxique néonatal conduit chez le rat adulte à de l’HTA, une dysfonction endothéliale et une rigidité artérielle, éléments de vieillissement vasculaire. Nous émettons l'hypothèse qu'un stress hyperoxique néonatale conduit à long terme à l'altération de la structure vasculaire et à un vieillissement vasculaire précoce. Nous avons démontré une diminution de la prolifération cellulaire, une capacité angiogénique altérée, des dommages à l’ADN et une augmentation de l’expression de protéines de sénescences (des indices de sénescence cellulaire) au-delà de la période néonatale suite à une exposition brève à l’O2 au niveau vasculaire dans un modèle animal (ratons Sprague-Dawley exposés à 80 % d’O2 du 3ème au 10ème jour de vie comparés à des ratons restés à l’air ambiant) et cellulaire (cellules musculaires lisses d'aortes thoraciques d'embryon de rat exposées à 40% O2 pendant 24h ou 48h, puis remises en normoxie pendant 96h). De plus, des altérations des composants de la structure vasculaire indiquant un remodelage vasculaire aortique ont été mises en évidence. Ces changements précèdent tous l’HTA et la dysfonction vasculaire observées dans le modèle animal à l’âge adulte et pourraient y contribuer. L’étude de jeunes adultes nés < 29 semaines comparés à des jeunes adultes nés à terme indique une augmentation de marqueurs de rigidité artérielle (indices d’un vieillissement vasculaire précoce) chez la population prématurée. L’ensemble des résultats démontre un vieillissement vasculaire précoce après une exposition néonatale transitoire à un stress hyperoxique permettant une meilleure compréhension des mécanismes physiopathologiques impliqués dans la survenue des troubles vasculaires retrouvés chez l’adulte et contribue à la mise en place de moyens de prévention chez des patients prématurés.
The scope of this thesis is developmental programming of arterial high blood pressure (HBP) hypertension through early neonatal stimuli that may alter vascular development. Premature newborns have decreased antioxidant defenses compared to term babies and are exposed upon birth to high oxygen (O2) concentration, causing reactive oxygen species (ROS) production. Long term vascular consequences of ROS related damage during the neonatal period and the mechanisms involved remain unknown. Recent data from the laboratory show that neonatal hyperoxic stress leads in adult rat to HBP, endothelial dysfunction and arterial rigidity, characteristic features of vascular aging. We hypothesize that a neonatal hyperoxic stress leads to long term vascular structure alteration explained by an early aging of the vascular system. We showed a decreased proliferation rate, an altered angiogenic capacity, as well as long term DNA damage and increased expression of senescence proteins at a vascular level following O2 exposure in the animal (male Sprague-Dawley pups kept at 80% O2 from postnatal days 3 to 10 vs. rats remained in room air) and cellular models (embryonic vascular smooth muscle cells from rat thoracic aorta exposed to 40% O2 for 24h or 48h followed by 96h recovery in control conditions). In addition, alterations of vascular structure components indicating vascular remodeling was shown before the onset of the HBP at adult age. Those changes precede the HBP and vascular dysfunction observed in our animal model at adult age and could contribute to them. Study of young adults born before 29 weeks vs. young adults born at term showed that young adults born preterm present indices of arterial stiffness vs. term controls. Results of the present thesis demonstrate a major role of premature vascular aging in the surge of vascular diseases in adulthood and contribute to a better understanding of the patho-physiological mechanisms involved and could put into practice new prevention strategies among preterm patients.

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Molenat-Sérafin, Florence. "Effets de l'oxygène, hypoxie et hyperoxie, sur le système cardio-vasculaire." Aix-Marseille 2, 2003. http://www.theses.fr/2003AIX20674.

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Le métabolisme humain est oxygéno-dépendant ; l'oxygène est aussi responsable d'effets toxiques par le biais de radicaux libres. Nous avons étudié par Echocardiographie et Doppler la tolérance cardio-vasculaire de sujets sains en milieux enrichis ou appauvris en oxygène. Nous n'avons pas retrouvé d'atteintes majeures des propriétés intrinsèques du cœur. La contractilité était préservée en hypoxie, et peu altérée en hyperoxie. Il existait, en hypoxie et en hyperoxie, une diminution du remplissage rapide du ventricule gauche liée à une baisse de la précharge. La vasomotricité était inchangée en hypoxie ; mais il existait une vasoconstriction hyperoxique marquée, sans pouvoir conclure si elle était pathologique ou adaptée à l'augmentation de l'oxygène artériel. Enfin, dans le cas des expérimentations en hypobarie, nous avons montré que la détection des bulles circulantes par échographie-Doppler pouvait optimiser les procédures de sécurité en proposant des procédures individuelles
Human metabolism depends on the presence of oxygen. However, oxygen may have some toxic effects via the radical oxygen species. We studied, using Echocardiography and Doppler, the cardiovascular tolerance in healthy subjects submitted to environments with high or poor oxygen content. Intrinsic properties of the heart seemed well preserved. Cardiac contractility was unchanged in hypoxia and poorly decreased in hyperoxia. We observed that left ventricle (LV) filling was modified with a lower early filling, in hypoxia and hyperoxia, because of a decreased LV preload. Arterial tone was unchanged in hypoxia, but there was an marked arterial vasoconstriction in hyperoxia. However, we could not conclude weither it was pathological or adapted to the increased arterial content. At least, in hypobaric experiments, we demonstrated that the detection of circulating bubbles, using echocardiography and Doppler, could improve the security procedure, using individual procedures

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Deffert, Delbouille Christine. "Modèles murins déficients en NOX1 ou NOX2 : applications physiopathologiques." Université Joseph Fourier (Grenoble), 2009. http://www.theses.fr/2009GRE10335.

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Les espèces réactives de l'oxygène ou ROS sont des molécules dérivées de l'oxygène produites "de manière professionnelle" par les NADPH oxydases (NOX). Ces enzymes utilisent l'oxygène comme acceptateur d'électrons afin de les transférer à travers les membranes. Le produit de cette réaction est l'anion superoxyde et ses dérivés : les espèces réactives de l'oxygène (ROS). La famille des NADPH oxydases est composée che l'Homme de 7 membres : NOX1 à NOX5, DUOX1 et DUOX2. Bien que les structures des différentes isoformes des NOX soient très homologues, leurs mécanismes d'activation et leurs distributions tissulaires, cellulaires et subcellulaires et en conséquence, leurs donctions physiologiques sont très différents. Leurs rôles physiologiques mais aussi pathologiques ont été très souvent déterminés à l'aide de modèles murins transgéniques. Le travail présenté dans cette thèse a eu pour but de déterminer deux nouveaux rôles de NOX1 dans des pathologies humaines : l'hypertension artérielle et le syndrome de détresse respiratoire. Dans un second temps, nous avons également évalué le rôle anti-inflammatoire de NOX2 en utilisant comme modèle des souris déficientes en Nox2. NOX1 a été implqué dans l'hypertension artérielle induite par l'angiotensine II. Dans cette étude, il a été démontré que les ROS générés par NOX1 sont impliqués dans la formation des anévrysmes aortiques induits par l'angiotensine II. Alors que l'activation de NOX1 par l'angiotensine II via son récepteur AT1 est un phénomène bien connu, nous avons démontré que NOX1 est capable également de réguler la présence du récepteur AT1 à la membrane plasmique. Les poumons soumis à des conditions d'hyperoxie vont être exposés à des concentrations importantes de ROS favorisant et exacerbant les lésions pulmonaires. Lors de cette étude, nous avons démontré à l'aide de souris déficientes en Nox1 que cette NADPH oxydase uniquement est impliquée dans la génération des ROS induite par l'hyperoxie. La maladie granulomateuse septique ou CGD est un syndrome d'immunodéficience dû à la présence de mutations au niveau du gène codant pour NOX2. Associées aux infections, des réactions inflammatoires exacerbées sont observées chez les patients CGD et ont un impact sur la morbidité. Dans cette étude, nous avons déterminé qu'une des origines possibles de l'inflammation en l'absence de NOX2 est le β-glycan. Cette hyperinflammation observée dans un modèle inflammatoire cutané chez les souris déficientes en Nox2 est associée à de fortes quantités de TNFα, l'augmentation de cette cytokine pro-inflammatoire n'est pas le principal médiateur les lésions inflammatoires induites par les β-glycans et l'absence de Nox2. Le traitement des patients CGD par des bloqueurs du TNFα ne semble donc pas recommandé. D'un autre côté, il semble que les molécules capables de bloquer les effets des β-glycans sont à considérer comme des cibles potentielles pour la recherche de molécules anti-inflammatoires spécifiques et le développement de nouvelles stratégies thérapeutiques et préventives pour les patients CGD
Reactive oxygen species (ROS) are molecules derived from oxygen. They are generated by professional NADPH oxidases (NOX). The NOX family is proteins that transfer electrons across biological membranes. In general, the electron acceptor is oxygen and the product of the electron transfer reaction is superoxide. Seven NOXs proteins has been described and all of them generate or ROS. Despite their similar structure and enzymatic function, NOX family enzymes differ in their mechanism of activation, their tissues, cellular and subcellular localizations and in consequence their physiological functions. Physiological and pathological roles of NOX enzymes are usually discovered in transgenic mouse models. The goal of this thesis was to determine two new roles of NOX1 in human diseases : hypertension and respiratory distress syndrome using Nox1-deficient mice. Secondly, we have evaluated the anti-inflammatory role of NOX2 using Nox2-deficient mice. NOX1 has been involved in angiotensin II-induced hypertension. In this study, it has been demonstrated that NOX1-generated ROS have also implicated in angiotensin II-induced aneurysms. They can regulate the metallo-protease activity and fibrosis. NOX1 is activated by angiotensin II receptor (AT1) engagement. We have demontrated that NOX1 also regulates the AT1 expression to the plasma membrane. NOX1 seems to be a possible therapeutical target in hypertension and aneurysm formation. The respiratory distress syndrome especially in premature babies is characterized by immature lung development. During respiratory distress syndrome treatment with mechanical ventilation and high oxygen concentration, the lungs are exposed to increased oxidative stress leadings to pulmonary injury. During this study, we have demonstrated that Nox1 but not Nox2 participates to hyperoxie-induced lung injury. In Nox1-deficient mice, decreased ROS generation reduce cell death in alveolar epithelial and endothelial cells. NOX1 seems also to be possible therapeutical target in respiratory distress syndrome. Chronic granulomatous disease (CGD) is an immunodeficiency syndrome due to mutations in gene gp91(phox) coding for NOX2 protein. In consequence, CGD patients suffer from severe and recurrent infections. Indeed, they present hyperinflammatory response which plays a role in the morbidity of the disease. During this study, we have demonstrated that a possible stimulus of this CGD inflammatory complication is the β-glycans, in Nox2-deficient mice. These glucose polymers induce inflammatory that cannot be resolved in absence of NOX2. Also, CGD hyperinflammation is characterized by important TNFα production. But the blockage of TNFα has not dampened CGD hyperinflammation. In the other hand, the blockage of the principal β-glycans receptor, dectin-1 pharmacologically or genetically, has reduced significantly CGD inflammation. These data constiture new therapeutical target in CGD inflammatory syndrome

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Gösele, Michael. "Effekte einer frühen Beatmung mit reinem Sauerstoff auf histomorphologische Parameter von Lunge und Leber im Langzeitmodell des septischen Schocks beim Schwein." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-65831.

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Kühn, Christine [Verfasser]. "Effekte einer intermittierenden Hyperoxie auf die mitochondriale Atmung in Alveolarmakrophagen / Christine Kühn." Ulm : Universität Ulm, 2016. http://d-nb.info/1105559882/34.

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Bock, Ulf Bastian [Verfasser]. "Auswirkung von normobarer Hyperoxie auf die mitochondriale Atmung von Alveolarmakrophagen / Ulf Bastian Bock." Ulm : Universität Ulm. Medizinische Fakultät, 2016. http://d-nb.info/1081432187/34.

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Books on the topic "Hyperoxie"

1

A, Sher Neal, ed. Surgery for hyperopia. Thorofare, NJ: Slack Inc., 2004.

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A, Sher Neal, ed. Surgery for hyperopia and presbyopia. Baltimore: Williams & Wilkins, 1997.

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Afanasʹev, Igor B. Superoxide ion: Chemistry and biological implications. Boca Raton: CRC Press, 1991.

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Roberto, Pinelli, and Pascucci Stephen, eds. Conductive keratoplasty: A primer. Thorofare, NJ: SLACK, 2005.

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Judd, Sandra J. Eye care sourcebook: Basic consumer health information about vision and disorders affecting the eyes and surrounding structures, including facts about hyperopia, myopia, presbyopia, astigmatism, cataracts, macular degeneration, glaucoma, and other disorders of the cornea, retina, macula, conjunctiva, and optic nerve; along with guidelines for recognizing and treating eye emergencies, advice about protecting the eyes at work, home, and play, tips for living with low vision ... 5th ed. Detroit, MI: Omnigraphics, 2012.

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Sifringer, Marco. Hyperoxie- und Trauma-Induzierte Schädigungen Im Unreifen Gehirn. Südwestdeutscher Verlag für Hochschulschriften AG & Company KG, 2012.

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Baqué, Ute. Untersuchungen zum einfluss einer Peep-Beatmung auf den PAO₂ in Hyperoxie. 1994.

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Petersen, Carsten. Die Auswirkung arterieller Hyperoxie auf die Sauerstoffversorgung des Skelettmuskels: Tierexperimentelle Untersuchung. 1988.

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Anders, Bernhard. Der Einfluss einer Normobaren Hyperoxie auf die O₂-Versorgung von Herz und Leber. 1996.

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Tsubota, Kazuo, Dimitri T. Azar, Brian S. Boxer Wachler, and Douglas Koch. Hyperopia and Presbyopia. Taylor & Francis Group, 2003.

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Book chapters on the topic "Hyperoxie"

1

Burges, A., A. M. Allmeling, C. Hammer, and F. Krombach. "Hyperoxie-induzierte Veränderungen der Alveolarmakrophagenfunktion." In Chirurgisches Forum ’91 für experimentelle und klinische Forschung, 365–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76513-1_75.

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Pepperl, Sonja, M. Dörger, and F. Krombach. "Hyperoxie steigert die LPS- and IFN-gamma-induzierte NO-Freisetzung durch Alveolarmakrophagen." In Deutsche Gesellschaft für Chirurgie, 473–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60133-0_92.

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Pepperl, S., M. Dörger, F. Ringel, C. Kupatt, and F. Krombach. "Bedeutung von ROS und NF-κB/AP-1 für die iNOS-Induktion unter Hyperoxie." In Deutsche Gesellschaft für Chirurgie, 369–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56698-1_95.

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Lamm, K., E. Lüllwitz, C. Lamm, and H. Lamm. "Durchblutung, Sauerstoffversorgung und Funktion des Innenohres während arterieller Hyperoxie und Hypoxie — Eine experimentelle Studie." In Teil II: Sitzungsbericht, 44–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84592-5_16.

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Meier, Jens, Konrad Messmer, and Oliver Habler. "Hyperoxic Hemodilution." In Alternatives to Blood Transfusion in Transfusion Medicine, 450–57. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444319583.ch37.

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Klaproth, Oliver K., and Thomas Kohnen. "Hyperopia." In Encyclopedia of Ophthalmology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-642-35951-4_381-4.

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Klaproth, Oliver K., and Thomas Kohnen. "Hyperopia." In Encyclopedia of Ophthalmology, 909–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_381.

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Zhang, Jun, Ling-Lei Kong, and Guan-Hua Du. "Hyperoside." In Natural Small Molecule Drugs from Plants, 697–701. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8022-7_113.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "Hyperopia." In Encyclopedia of Molecular Mechanisms of Disease, 913–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8830.

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Haeussler-Sinangin, Yesim, and Thomas Kohnen. "Hyperopic Shift." In Encyclopedia of Ophthalmology, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-642-35951-4_435-4.

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Conference papers on the topic "Hyperoxie"

1

Borger, Moritz, Nora Künzel, Christoph Bührer, and Stefanie Endesfelder. "Effekte von Hypoxie, Hyperoxie und Dexmedetomidin auf Kardiomyozyten der Ratte." In Abstracts zur 49. Jahrestagung der Gesellschaft fär Neonatologie und Pädiatrische Intensivmedizin (GNPI). Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1769242.

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Gallert, Markus, Meray Serdar, Mandana Rizazad, Karina Kempe, Josephine Herz, Ursula Felderhoff-Müser, and Ivo Bendix. "Effekt einer pränatalen Infektion/Entzündung in Kombination mit postnataler Hyperoxie auf das neonatale Gehirn." In Abstracts zur 49. Jahrestagung der Gesellschaft fär Neonatologie und Pädiatrische Intensivmedizin (GNPI). Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1769282.

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Serdar, Meray, Karina Kempe, Mandana Rizazad, Josephine Herz, Ursula Felderhoff-Müser, and Ivo Bendix. "Untersuchung der therapeutischen Wirkung von Stammzellen (MSZ) auf primäre Oligodendrozyten und hippocampale Neurone nach einer Hyperoxie." In Abstracts zur 49. Jahrestagung der Gesellschaft fär Neonatologie und Pädiatrische Intensivmedizin (GNPI). Georg Thieme Verlag KG, 2023. http://dx.doi.org/10.1055/s-0043-1769252.

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Bizios, R., L. A. Holleran, T. P. Ladd, and R. D. Iveson. "EFFECTS OF HYPER0XIC AND HYPOXIC CONDITIONS ON ALBUMIN TRANSPORT ACROSS CULTURED ENDOTHELIAL MONOLAYERS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643361.

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Transport of albumin across cultured bovine pulmonary artery endothelial monolayers was studied under control (ambient air), hyperoxic (95% O2, 5% CO2) and hypoxic (95% N2, 5% CO2) conditions at 37°C over 3 hours. The experimental system consisted of two compartments separated by the endothelial monolayer grown to confluence on a gelatinized polycarbonate membrane (0.8 μm pore diameter). Albumin (4 gm% in PBS) solution and PBS buffer were placed on the luminal and abluminal sides of the confluent endothelial monolayer respectively. Albumin concentrations in the abluminal compartment at various time intervals were determined (Lowry assay) and the results are shown in the table.Compared to control, exposure to hyperoxia resulted in increased albumin transendothelial transport by one order of magnitude for time intervals up to 1 hr, and by over 50% for later times. In contrast albumin transendothelial transport under hypoxic conditions was comparable to the results obtained under control conditions. The results of this study indicate that hyperoxia greatly affects the transport properties of endothelium. (Supported by the Whitaker Foundation.)

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Wong, S. T., J. G. Sivak, A. K. Bal, M. G. Callender, and A. J. Bakelaar. "Changes in Amacrine Cell Numbers and Morphology in Response To Induced Myopia and Hyperopia." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1998. http://dx.doi.org/10.1364/vsia.1998.suc.2.

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Myopia and hyperopia have been artificially induced in animal models by various manipulations of their early visual environment. Ametropias have been produced using lid suture1, changing illumination levels (dark-rearing2, constant light3, dim lighting4), intra-ocular injections5, treatment with defocussing lenses6, and the application of translucent occluders7. Abnormal ocular growth appears to be a major factor that causes ametropia. Myopic eyes are enlarged, while hyperopic eyes are smaller compared to control eyes. Changes in the sclera8, choroid9, and orbital bone10 surrounding the affected eyes also reflect abnormal growth mechanisms. Various studies11,12,13 suggest that the signal or signals which control eye growth may arise from within the retina itself. It has been suggested that retinal amacrine cells play a role in mediating ocular growth8. This study examines how dopaminergic and serotonergic amacrine cells are quantitatively and qualitatively affected by induced myopia and hyperopia.

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Sivak, Jacob G., Elizabeth L. Irving, Margot E. Andison, and Murchinson Callender. "Inducing refractive errors in birds." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/oam.1991.tuy1.

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Numerous studies have shown that depriving the eye of the young chicken of clear form vision always results in myopia. Deprivation is usually achieved by the use of a translucent goggle over one eye. However, manipulation of the early visual environment of birds does not always produce myopia. The application of lenses to produce positive and negative defocus of the image of the young chick eye results in the formation of hyperopia and myopia, respectively. Preliminary results show that astigmatic defocus can produce astigmatic refractive states. Also, the application of a translucent goggle to the eye of the young American kestrel (Falco sparverius) produces both hyperopia and myopia, although myopia predominates. Furthermore, the normal hatchling kestrel eye is myopic and not hyperopic as is the hatchling chick. Hence, emmetropia is approached from opposite directions in these two species during the first few days after hatching. These results indicate that models of refractive error development of the bird eye should be able to account for all refractive conditions.

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Lane, Ben C. "Diet-responsive blood-indexed risk factor for high myopia." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/oam.1990.tuy24.

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Previously 1 reported highly significant depression of the chromium-to-vanadium ratio in the nape hair of patients with myopia. It is associated with depressed accommodation and elevated intraocular pressure, both of which are associated with depression of insulin potentiation of glucose uptake by ciliary-muscle insulin receptors.1,2 In this double-masked cohort-panel study, chromium (Cr) and vanadium (V) were measured in red blood cells (erythrocytes). Of the first 184 patients, 27 were myopic (3 diopters) and 14 were hyperopic (1.25 diopter). I excluded patients less than 20 years old, patients taking chromium supplements, patients taking 1 g or more of ascorbic acid per day, aphakic patients, and patients with cataracts. Erythrocytechromium/erythrocytevanadi um (ECr/EV) ratios and ECr distributions and means were significantly lower in the patients with miopia than in the patients with hyperopia: mean SD ECr/EV = 0.150 0.150 for the myopic patients versus 0.731 0.472 for the hyperopic patients (t = 4.488, p), and ECr = 70.1 53.9 ng/ml for the myopic patients and 256.7 160.0 for the hyperopic patients. Foods rich in chromium include most unprocessed naturally sweet or starchy foods. Foods rich in vanadium include chocolate, kelp, mushrooms, most U.S. chow-fed poultry, and seafood larger than herring. To my knowledge, this is the first report of this red-blood-cell-indexed effect on human refractive development.

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Munger, Rejean, Evanne J. Casson, and W. Bruce Jackson. "Topography and optical performance of the cornea following hyperopic Excimer PRK." In Vision Science and its Applications. Washington, D.C.: Optica Publishing Group, 1997. http://dx.doi.org/10.1364/vsia.1997.fc.1.

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Visual performance after refractive surgery depends critically on the optical quality of the post-operative cornea. To understand subtle visual problems that cannot be corrected by optical means we must go beyond the paraxial refractive power of the cornea and fully characterize its optical properties. Research is also required into the relationship between the shape of the cornea and visual performance after PRK. As a first step towards a better description of the optical characteristics of PRK corneas we are developing ray tracing methods, which use corneal topography as the surface descriptor, to calculate their optical properties. The Eye Institute is also involved in a pilot study to evaluate the VISX “STAR” Excimer laser for PRK treatment of hyperopia. In this paper we present data on (a) corneal optical quality, (b) corneal topography (ablation profile), and (C) visual acuities for 2 patients followed for 6 months after a hyperopic Excimer PRK surgery.

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Skavronskaya, M. V., and I. N. Fedina. "THE STRUCTURE OF PRIORITY FORMS OF SOMATIC PATHOLOGY AND DISEASES OF VISUAL ORGAN IN EMPLOYEES OF TRANSPORT ENTERPRISES." In The 17th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2023). FSBSI «IRIOH», 2023. http://dx.doi.org/10.31089/978-5-6042929-1-4-2023-1-423-427.

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Due to the multifactorial impact of the working and environmental environment and the labor process on the body of drivers, the identification of priority pathology in order to preserve high visual functions is an important task to preserve human resources and ensure transport safety. The study of the structure of diseases of the eye and its accessory apparatus, as well as priority forms of somatic pathology, was carried out through a retrospective analysis of 4,240 outpatient records of professional drivers of vehicles of all categories who underwent periodic medical examination (PME) at the clinic of the Izmerov Research Institute of Occupational Health in 2020‑2022. Among the surveyed drivers, 32.1% suffer from obesity, arterial hypertension and essential hypertension established were diagnosed in 1.3 and 16.6% of drivers, respectively; diabetes mellitus — in 2.7%; сardiac ischemia — in 0.9%. The structure of the pathology of the organ of vision of employees of a transport enterprise was determined based on the results of periodic medical examinations in 2021‑2022: 76.8% of drivers of vehicles of various categories have a pathology of the organ of vision; the leading group of ophthalmic pathologies are refractive errors, among which hyperopia and hyperopic astigmatism prevail (28.9% of the number of drivers); there was a trend for a significant increase in cases of hyperopic refraction after 40 years; the proportion of workers with a refractive error or a combination of them in the group of drivers is higher than in the general structure of all cases of completed medical examination.

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Vitiello, Peter, and Elliot Bloom. "Hyperoxic Modification Of Thioredoxin-Dependent Pathways." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5960.

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Reports on the topic "Hyperoxie"

1

Mehm, William J. Effect of Barbiturates and Hyperoxia on Lipid Peroxidation in Hypoxic Neurons. Fort Belvoir, VA: Defense Technical Information Center, April 1993. http://dx.doi.org/10.21236/ada278467.

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Dougherty, J. H., Eckenhoff Jr., Hunter R. G., Jr W. L., J. W. Parker, and D. J. Styer. Hyperbaric and Hyperoxic Effects on Pulmonary Function During Air Saturation Dives. Fort Belvoir, VA: Defense Technical Information Center, July 1985. http://dx.doi.org/10.21236/ada418606.

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Shykoff, B. Incidence of CNS Oxygen Toxicity with Mild Hyperoxia: A Literature and Data Review. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada607392.

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Zupan, Michael F., Dustin R. Bakkie, Jennifer A. Malagon, Jessica A. Malagon, and Kristin Perdue. Comparison of the 1.5 Mile Run Times at 7,200 Feet and Simulated 850 Feet in a Hyperoxic Room. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada567837.

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Zupan, Michael F., Dustin R. Bakkie, Jennifer A. Malagon, Jessica A. Malagon, and Kristin Perdue. Comparison of the 1.5 Mile Run Times at 7,200 Feet and Simulated 850 Feet in a Hyperoxic Room. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada580886.

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