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Littérature scientifique sur le sujet « CMRO2 »

Auteur : Grafiati
Publié le 29 mars 2025

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Articles de revues sur le sujet "CMRO2"

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Jain, Varsha, Erin M. Buckley, Daniel J. Licht, Jennifer M. Lynch, Peter J. Schwab, Maryam Y. Naim, Natasha A. Lavin et al. « Cerebral Oxygen Metabolism in Neonates with Congenital Heart Disease Quantified by MRI and Optics ». Journal of Cerebral Blood Flow & ; Metabolism 34, no 3 (11 décembre 2013) : 380–88. http://dx.doi.org/10.1038/jcbfm.2013.214.

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Neonatal congenital heart disease (CHD) is associated with altered cerebral hemodynamics and increased risk of brain injury. Two novel noninvasive techniques, magnetic resonance imaging (MRI) and diffuse optical and correlation spectroscopies (diffuse optical spectroscopy (DOS), diffuse correlation spectroscopy (DCS)), were employed to quantify cerebral blood flow ( CBF) and oxygen metabolism ( CMRO2) of 32 anesthetized CHD neonates at rest and during hypercapnia. Cerebral venous oxygen saturation ( Sv O2) and CBF were measured simultaneously with MRI in the superior sagittal sinus, yielding global oxygen extraction fraction ( OEF) and global CMRO2 in physiologic units. In addition, microvascular tissue oxygenation ( StO2) and indices of microvascular CBF (BFI) and CMRO2 ( CMRO2i) in the frontal cortex were determined by DOS/DCS. Median resting-state MRI-measured OEF, CBF, and CMRO2 were 0.38, 9.7 mL/minute per 100 g and 0.52 mL O2/minute per 100 g, respectively. These CBF and CMRO2 values are lower than literature reports for healthy term neonates (which are sparse and quantified using different methods) and resemble values reported for premature infants. Comparison of MRI measurements of global Sv O2, CBF, and CMRO2 with corresponding local DOS/DCS measurements demonstrated strong linear correlations ( R2=0.69, 0.67, 0.67; P<0.001), permitting calibration of DOS/DCS indices. The results suggest that MRI and optics offer new tools to evaluate cerebral hemodynamics and metabolism in CHD neonates.
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Klementavicius, Richard, Edwin M. Nemoto et Howard Yonas. « The Q10 ratio for basal cerebral metabolic rate for oxygen in rats ». Journal of Neurosurgery 85, no 3 (septembre 1996) : 482–87. http://dx.doi.org/10.3171/jns.1996.85.3.0482.

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✓ Previously the authors showed that hypothermia exerts a greater effect on the cerebral metabolic rate for oxygen (CMRO2) that is associated with the maintenance of cellular viability, or “basal” CMRO2, than on electroencephalogram (EEG)-associated CMRO2 or “functional” CMRO2. On the basis of their findings, the authors hypothesized that the ratio of CMRO2 over a 10°C temperature range (Q10) for basal CMRO2 was greater than that for functional and total CMRO2. They tested their hypothesis by determining the Q10 for basal CMRO2 from 38°C to 28°C. They measured whole-brain cerebral blood flow (CBF) and CMRO2 in six rats during progressive hypothermia at a brain temperature of 38°C and, after induction of an isoelectric EEG signal (50 µV/cm) with thiopental sodium, they repeated the measurements at 38°C, 34°C, 30°C, and 28°C. In a control group (five rats), six sequential measurements of CBF and CMRO2 were made while the animals were anesthetized by 0.5% isoflurane/70% N2O/30% O2 at a brain temperature of 38°C over a time span equivalent to the hypothermic group, that is, approximately 3 hours. The Q10 for basal CMRO2 calculated over 38°C to 28°C was 5.2 ± 0.92. However, the decrease in basal CMRO2 between 38°C and 28°C was nonlinear on a log plot, revealing a two-component response: a high temperature sensitivity component between 38°C and 30°C with a Q10 of 12.1, and a lower temperature sensitivity component between 30°C and 28°C with a Q10 of 2.8. The combined overall Q10 for basal CMRO2 between 38° and 28°C was 5.2. The energy-requiring processes associated with these high and low temperature sensitivity components of basal CMRO2 have yet to be identified.
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Zhu, Xiao-Hong, Nanyin Zhang, Yi Zhang, Kâmil Uğurbil et Wei Chen. « New Insights into Central Roles of Cerebral Oxygen Metabolism in the Resting and Stimulus-Evoked Brain ». Journal of Cerebral Blood Flow & ; Metabolism 29, no 1 (10 septembre 2008) : 10–18. http://dx.doi.org/10.1038/jcbfm.2008.97.

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The possible role of oxygen metabolism in supporting brain activation remains elusive. We have used a newly developed neuroimaging approach based on high-field in vivo17O magnetic resonance spectroscopic (MRS) imaging to noninvasively image cerebral metabolic rate of oxygen (CMRO2) consumption in cats at rest and during visual stimulation. It was found that CMRO2 increases significantly (32.3% ± 10.8%, n = 6) in the activated visual cortical region as depicted in blood oxygenation level dependence functional maps; this increase is also accompanied by a CMRO2 decrease in surrounding cortical regions, resulting a smaller increase (9.7% ± 1.9%) of total CMRO2 change over a larger cortical region displaying either a positive or negative CMRO2 alteration. Moreover, a negative correlation between stimulus-evoked percent CMRO2 increase and resting CMRO2 was observed, indicating an essential impact of resting brain metabolic activity level on stimulus-evoked percent CMRO2 change and neuroimaging signals. These findings provide new insights into the critical roles of oxidative metabolism in supporting brain activation and function. They also suggest that in vivo17O MRS imaging should provide a sensitive neuroimaging modality for mapping CMRO2 and its change induced by brain physiology and/or pathologic alteration.
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Meyer, E., J. L. Tyler, C. J. Thompson, C. Redies, M. Diksic et A. M. Hakim. « Estimation of Cerebral Oxygen Utilization Rate by Single-Bolus 15O2 Inhalation and Dynamic Positron Emission Tomography ». Journal of Cerebral Blood Flow & ; Metabolism 7, no 4 (août 1987) : 403–14. http://dx.doi.org/10.1038/jcbfm.1987.83.

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This study shows that regional CMRO2 can be estimated by means of nonlinear regression using dynamic positron emission tomographic data acquired during 1 min following single-bolus inhalation of 15O2. The feasibility of simultaneous estimation of CBF, cerebral blood volume (CBV), oxygen extraction ratio (OER), and CMRO2 was assessed by simulations using the model of Mintun et al. Four oxygen metabolic measurements, each consisting of a CBF, CBV, and 15O2 bolus study, were carried out on three volunteers. Regional values for CBF, CBV, OER, and CMRO2 were derived in two ways: from the fits of the time-activity curves of the dynamic 15O2 bolus study alone [CMRO2(fit)] and from the three separate studies [CMRO2 (control)]. For the 56 regions of interest analyzed, using a fit interval of 60 s, CMRO2(fit) was 93.4 ± 7.8% of CMRO2(control) (mean ± SD) with a correlation coefficient of r = 0.95. CMRO2(control) ranged from 87 to 290 μmol/min/100 g. Individual simultaneous estimates of CBF, CBV, and OER were not reliable. Finally, we found that the validity of the model was limited in practice to the first minute after tracer inhalation.
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Thomsen, Kirsten, Henning Piilgaard, Albert Gjedde, Gilles Bonvento et Martin Lauritzen. « Principal Cell Spiking, Postsynaptic Excitation, and Oxygen Consumption in the Rat Cerebellar Cortex ». Journal of Neurophysiology 102, no 3 (septembre 2009) : 1503–12. http://dx.doi.org/10.1152/jn.00289.2009.

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One contention within the field of neuroimaging concerns the character of the depicted activity: Does it represent neuronal action potential generation (i.e., spiking) or postsynaptic excitation? This question is related to the metabolic costs of different aspects of neurosignaling. The cerebellar cortex is well suited for addressing this problem because synaptic input to and spiking of the principal cell, the Purkinje cell (PC), are spatially segregated. Also, PCs are pacemakers, able to generate spikes endogenously. We examined the contributions to cerebellar cortical oxygen consumption (CMRO2) of postsynaptic excitation and PC spiking during evoked and ongoing neuronal activity in the rat. By inhibiting excitatory synaptic input using ionotropic glutamate receptor blockers, we found that the increase in CMRO2 evoked by parallel fiber (PF) stimulation depended entirely on postsynaptic excitation. In contrast, PC spiking was largely responsible for the increase in CMRO2 when ongoing neuronal activity was increased by γ-aminobutyric acid type A receptor blockade. In this case, CMRO2 increased equally during PC spiking with excitatory synaptic activity as during PC pacemaker spiking without excitatory synaptic input. Subsequent inhibition of action potential propagation and neurotransmission by blocking voltage-gated Na+-channels eliminated the increases in CMRO2 due to PF stimulation and increased PC spiking, but left a large fraction of CMRO2, i.e., basal CMRO2, intact. In conclusion, whereas basal CMRO2 in anesthetized animals did not seem to be related to neurosignaling, increases in CMRO2 could be induced by all aspects of neurosignaling. Our findings imply that CMRO2 responses cannot a priori be assigned to specific neuronal activities.
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Rodgers, Zachary B., John A. Detre et Felix W. Wehrli. « MRI-based methods for quantification of the cerebral metabolic rate of oxygen ». Journal of Cerebral Blood Flow & ; Metabolism 36, no 7 (18 avril 2016) : 1165–85. http://dx.doi.org/10.1177/0271678x16643090.

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The brain depends almost entirely on oxidative metabolism to meet its significant energy requirements. As such, the cerebral metabolic rate of oxygen (CMRO2) represents a key measure of brain function. Quantification of CMRO2 has helped elucidate brain functional physiology and holds potential as a clinical tool for evaluating neurological disorders including stroke, brain tumors, Alzheimer’s disease, and obstructive sleep apnea. In recent years, a variety of magnetic resonance imaging (MRI)-based CMRO2 quantification methods have emerged. Unlike positron emission tomography – the current “gold standard” for measurement and mapping of CMRO2 – MRI is non-invasive, relatively inexpensive, and ubiquitously available in modern medical centers. All MRI-based CMRO2 methods are based on modeling the effect of paramagnetic deoxyhemoglobin on the magnetic resonance signal. The various methods can be classified in terms of the MRI contrast mechanism used to quantify CMRO2: T2*, T2′, T2, or magnetic susceptibility. This review article provides an overview of MRI-based CMRO2 quantification techniques. After a brief historical discussion motivating the need for improved CMRO2 methodology, current state-of-the-art MRI-based methods are critically appraised in terms of their respective tradeoffs between spatial resolution, temporal resolution, and robustness, all of critical importance given the spatially heterogeneous and temporally dynamic nature of brain energy requirements.
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Vazquez, Alberto L., Mitsuhiro Fukuda et Seong-Gi Kim. « Evolution of the Dynamic Changes in Functional Cerebral Oxidative Metabolism from Tissue Mitochondria to Blood Oxygen ». Journal of Cerebral Blood Flow & ; Metabolism 32, no 4 (1 février 2012) : 745–58. http://dx.doi.org/10.1038/jcbfm.2011.198.

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The dynamic properties of the cerebral metabolic rate of oxygen consumption (CMRO2) during changes in brain activity remain unclear. Therefore, the spatial and temporal evolution of functional increases in CMRO2 was investigated in the rat somato-sensory cortex during forelimb stimulation under a suppressed blood flow response condition. Temporally, stimulation elicited a fast increase in tissue mitochondria CMRO2 described by a time constant of ~ 1 second measured using flavoprotein autofluorescence imaging. CMRO2-driven changes in the tissue oxygen tension measured using an oxygen electrode and blood oxygenation measured using optical imaging of intrinsic signal followed; however, these changes were slow with time constants of ~ 5 and ~ 10 seconds, respectively. This slow change in CMRO2-driven blood oxygenation partly explains the commonly observed post-stimulus blood oxygen level-dependent (BOLD) undershoot. Spatially, the changes in mitochondria CMRO2 were similar to the changes in blood oxygenation. Finally, the increases in CMRO2 were well correlated with the evoked multi-unit spiking activity. These findings show that dynamic CMRO2 calculations made using only blood oxygenation data (e.g., BOLD functional magnetic resonance imaging (fMRI)) do not directly reflect the temporal changes in the tissue's mitochondria metabolic rate; however, the findings presented can bridge the gap between the changes in cellular oxidative rate and blood oxygenation.
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Vafaee, Manouchehr S., Albert Gjedde, Nasrin Imamirad, Kim Vang, Mallar M. Chakravarty, Jason P. Lerch et Paul Cumming. « Smoking Normalizes Cerebral Blood Flow and Oxygen Consumption after 12-Hour Abstention ». Journal of Cerebral Blood Flow & ; Metabolism 35, no 4 (21 janvier 2015) : 699–705. http://dx.doi.org/10.1038/jcbfm.2014.246.

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Acute nicotine administration stimulates [14C]deoxyglucose trapping in thalamus and other regions of rat brain, but acute effects of nicotine and smoking on energy metabolism have rarely been investigated in human brain by positron emission tomography (PET). We obtained quantitative PET measurements of cerebral blood flow (CBF) and metabolic rate of oxygen (CMRO2) in 12 smokers who had refrained from smoking overnight, and in a historical group of nonsmokers, testing the prediction that overnight abstinence results in widespread, coupled reductions of CBF and CMRO2. At the end of the abstention period, global grey-matter CBF and CMRO2 were both reduced by 17% relative to nonsmokers. At 15 minutes after renewed smoking, global CBF had increased insignificantly, while global CMRO2 had increased by 11%. Regional analysis showed that CMRO2 had increased in the left putamen and thalamus, and in right posterior cortical regions at this time. At 60 and 105 minutes after smoking resumption, CBF had increased by 8% and CMRO2 had increased by 11–12%. Thus, we find substantial and global impairment of CBF/CMRO2 in abstaining smokers, and acute restoration by resumption of smoking. The reduced CBF and CMRO2 during acute abstention may mediate the cognitive changes described in chronic smokers.
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Busija, D. W., C. W. Leffler et M. Pourcyrous. « Hyperthermia increases cerebral metabolic rate and blood flow in neonatal pigs ». American Journal of Physiology-Heart and Circulatory Physiology 255, no 2 (1 août 1988) : H343—H346. http://dx.doi.org/10.1152/ajpheart.1988.255.2.h343.

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We examined effects of hyperthermia on cerebral metabolic rate for oxygen (CMRO2) and cerebral blood flow (CBF) in anesthetized, newborn pigs (2–5 days old). CBF and CMRO2 were measured during normothermia (38 degrees C) and during hyperthermia induced by body heating (42 degrees C). During normothermia, total CBF was 32 +/- 3 ml.min-1.100 g-1 (n = 9), and CMRO2 was 1.34 +/- 0.08 ml O2.100 g-1.min-1 (n = 7). During hyperthermia, total CBF increased by 97 +/- 23% and CMRO2 by 65 +/- 24%. We also examined whether cerebral resistance vessels were responsive under these conditions. During hyperthermia, total CBF was 63 +/- 6 ml.min-1.100 g-1, and CMRO2 was 2.13 +/- 0.27 ml O2.100 g-1.min-1. During sustained hyperthermia, intravenous injection of 5 mg/kg of indomethacin decreased total CBF by 45 +/- 7% (n = 9), and CMRO2 fell by 55 +/- 10% (n = 5). We conclude that 1) hyperthermia increases CBF and CMRO2, and 2) the dilated cerebrovascular bed during hyperthermia still is responsive to a constrictor stimulus.
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Singh, Narendra C., Patrick M. Kochanek, Joanne K. Schiding, John A. Melick et Edwin M. Nemoto. « Uncoupled Cerebral Blood Flow and Metabolism after Severe Global Ischemia in Rats ». Journal of Cerebral Blood Flow & ; Metabolism 12, no 5 (septembre 1992) : 802–8. http://dx.doi.org/10.1038/jcbfm.1992.111.

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In a rat model of complete global brain ischemia (neck tourniquet) lasting either 3 min or 20 min, we monitored global CBF (sagittal sinus H2 clearance) and CMRO2 for 6 h to test the hypothesis that delayed postischemic hyperemia and uncoupling of CBF and CMRO2 occur depending on the severity of the insult. Early postischemic hyperemia occurred in both the 3-min and 20-min groups ( p < 0.05 vs. baseline values) and resolved by 15 min. Hypoperfusion occurred in the 3-min group between 15 and 60 min postischemia (≈23% reduction), and in the 20-min group from 15 to 120 min postischemia (≈50% reduction) ( p < 0.05), and then resolved. CMRO2 was not significantly different from baseline at any time after ischemia in the 3-min group. After 20 min of ischemia, however, CMRO2 was decreased (≈60%) throughout the postischemic period ( p < 0.05). At 5 min after ischemia, CBF/CMRO2 was increased in both groups but returned to baseline from 60 to 120 min postischemia. In the 3-min group, CBF/CMRO2 remained at baseline throughout the rest of the experiment. However, in the 20-min group, CBF/CMRO2 once again increased (≈100%), reaching a significant level at 180 min and remaining so for the rest of the 6-h period ( p < 0.05). These data demonstrate biphasic uncoupling of CBF and CMRO2 after severe (20 min) global ischemia in rats. This relatively early reemergence of CBF/CMRO2 uncoupling after 180 min of reperfusion is similar to that observed after prolonged cardiac arrest and resuscitation in humans.
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Thèses sur le sujet "CMRO2"

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Hoffmann, Stefan Heinrich [Verfasser], et Peter [Akademischer Betreuer] Bachert. « Lokalisierte Quantifizierung des zerebralen Sauerstoffumsatzes (CMRO2) mit der 17O-Magnetresonanztomographie / Stefan Heinrich Hoffmann ; Betreuer : Peter Bachert ». Heidelberg : Universitätsbibliothek Heidelberg, 2011. http://d-nb.info/1179783204/34.

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Boylan, Simon. « Cognitive effort, efficient coding and non-invasive fMRI measurement of their relation in sensorimotor responses ». Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0463.

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L'effort cognitif est une sensation subjective qui pousse les individus à éviter les tâches coûteuses. D'un point de vue biologique et évolutif, il est considéré comme un mécanisme destiné à préserver les ressources cognitives. Cependant, aucun consensus n'a été établi sur la nature de ces ressources. Puisque le cerveau est un organe de traitement de l'information, la théorie du codage efficient suggère que les ressources cognitives—quelle que soit leur nature—sont optimisées et dépendent du gain d'information lors du traitement d'une tâche.Cette hypothèse repose sur certains principes concernant le codage neuronal et le traitement de l'information. Premièrement, nous partons du principe que le cerveau traite l'information de manière bayésienne, mettant à jour ses modèles internes par des inférences entre les entrées sensorielles et les estimations antérieures. Deuxièmement, si les stimuli sont familiers, le codage neuronal efficient optimise alors le traitement de l’information. Si ces conditions sont remplies, nous pouvons estimer l'information traitée par le cerveau comme étant l'entropie relative entre estimations antérieures et postérieures, ou gain d’information ; de plus, l'énergie nécessaire pour traiter cette information étant optimisée, l'énergie dépensée pour accomplir la tâche devrait être proportionnelle à cette même quantité.Des mesures indirectes de cette relation ont été validées par pupillométrie, puisque la taille de la pupille est corrélée au taux d'information traité lors des tâches cognitives. Dans cette thèse, nous avons conçu des expériences pour valider davantage ce cadre théorique, en utilisant des mesures comportementales et de neuro-imagerie complémentaires.Nous avons mené trois expériences principales : deux tâches de poursuite visuomotrice par joystick et oculométrie, en parallèle de la pupillométrie, ainsi qu'une tâche de réponse à un stimulus (Hick-Hyman) en IRMf.La première étude examine la relation entre l'effort cognitif, la taille de la pupille et la prédiction visuomotrice dans ce cadre. En contrôlant les composantes informationnelles, telles que la prédictibilité, le retard, la vitesse et l'accélération de la cible, nous validons l'origine informationnelle de l'effort cognitif (NASA-TLX) et sa corrélation avec la taille de la pupille.La deuxième expérience a testé l’apprentissage implicite de trajectoires de cibles par oculométrie et contrôle manuel. et leur consolidation. Avec le même design que dans la première expérience, nous avons réalisé quatre sessions expérimentales sur deux jours consécutifs. Les participants apprenaient implicitement à mieux prédire les parties répétitives de la trajectoire, entraînant de meilleures performances et une dilatation pupillaire réduite.La dernière étude explorait la relation entre traitement de l'information et dissipation énergétique, en quantifiant le taux de consommation cérébrale en oxygène (CMRO2) lors d'une tâche de réponse à stimuli en IRMf (BOLD-ASL). La tâche de Hick-Hyman attribue un nombre différent de stimuli, en fonction de la complexité (entropie) de l'essai ou du bloc, à leurs boutons respectifs. Comme il existe une relation linéaire entre la quantité d'information traitée (entropie) et la performance (temps de réponse), nous avons émis l'hypothèse qu'il devrait exister une relation similaire entre la quantité d'information nécessaire pour accomplir une tâche et l'énergie qui lui est allouée. Nous avons abordé plusieurs défis techniques liés au calcul du CMRO2 dans ce contexte. Bien que nous ayons amélioré et automatisé le traitement des données, nous avons rencontré des obstacles importants qui nous ont empêchés de tirer une conclusion définitive sur notre hypothèse initiale
Cognitive effort is a ubiquitous subjective feeling of exertion that pushes people to avoid demanding tasks. From a biological and evolutionary point of view, mental effort is thought to be a mechanism intended to preserve cognitive resources. However, so far, no consensus on the nature of these resources has been established. Since the brain functions as an information-processing organ, efficient coding theory suggests that cognitive resources—whatever their nature—are optimized and should depend on information gain.This hypothesis assumes certain principles about neural coding and information processing. Firstly, we frame our work in the premise that the brain is a Bayesian information-processing machine, that updates internal models through inferences between inputs and previous beliefs. If stimuli are familiar and naturalistic, efficient neural coding can take place to optimize information coding and processing. If these conditions are met, then we can estimate the quantity of information computed by the brain as the relative entropy between prior and posterior beliefs, or information gain; moreover the quantity of energy needed to compute information being optimized, energy spent on a task should be proportional to this same quantity.Indirect measures of this relationship have been validated through pupillometry, as pupil size correlates with information rate during cognitive tasks. In this thesis, we designed experiments to further validate this information-theoretical framework, using complementary behavioral and neuroimaging measures.To assess this hypothesis, we conducted three key experiments : two joystick visuo-motor and oculomotor tracking tasks with pupillometry, and a response-to-stimulus (Hick-Hyman) task in fMRI.The first study investigates the relation between cognitive effort, pupil size and continuous visual-motor prediction under this information framework. By controlling information components of the target, such as predictability, lag, speed and acceleration, we can validate the information origin of cognitive effort (NASA-TLX) and its correlation with pupil size .The second experiment was developed to test the overnight memorization and implicitness of eye and hand continuous tracking. Using the same design as in the first experiment, we ran four experimental sessions, divided in joystick and eye tracking, on two consecutive days. We showed that participants implicitly learned to better predict repeating parts of the trajectory, which resulted in better performance and smaller pupil dilation.The last study was designed to investigate the relationship between information processing and energy dissipation in the brain by quantifying the cerebral metabolic rate of oxygen (CMRO2) during a response to stimulus task in fMRI (BOLD-ASL sequence). Hick-Hyman task maps a different number of stimuli to their response buttons, depending on the complexity (entropy) of the trial or block. As a linear relationship exists between the quantity of information processed (entropy) and the performance (response time) during the task, we hypothesized that there should be a similar relation between the quantity of information needed to accomplish a task and the energy allocated to do so. We addressed multiple technical issues related to CMRO2 computation in a cognitive task context. While we have improved and automatized the data analysis pipeline, we faced significant challenges that prevented us to reach a final conclusion on our initial hypothesis
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Bolar, Divya Sanam. « Magnetic resonance imaging of the cerebral metabolic rate of oxygen (CMRO₂) ». Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/57542.

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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, 2010.
This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student submitted PDF version of thesis.
Includes bibliographical references (p. 120-128).
Oxygen consumption is an essential process of the functioning brain. The rate at which the brain consumes oxygen is known as the cerebral metabolic rate of oxygen (CMRO₂). CMRO₂ is intimately related to brain health and function, and will change in settings of disease and functional activation. Accurate CMRO₂ measurement will enable detailed investigation of neuropathology and facilitate our understanding of the brain's underlying functional architecture. Despite the importance of CMRO₂ in both clinical and basic neuroscience settings, a robust CMRO₂ mapping technique amenable to functional and clinical MRI has not been established. To address this issue, a novel method called QUantitative Imaging of eXtraction of Oxygen and TIssue Consumption, or QUIXOTIC, is introduced. The key innovation in QUIXOTIC is the use of velocity-selective spin labeling to isolate MR signal exclusively from post-capillary venular blood on a voxel-by-voxel basis. This isolated signal can be related to venular oxygen saturation, oxygen extraction fraction, and ultimately CMRO₂. This thesis first explores fundamental theory behind the QUIXOTIC technique, including design of a novel MRI pulse sequence, explanation of the principal sequence parameters, and results from initial human experiences. A human trial follows, in which QUIXOTIC is used to measure cortical gray matter CMRO₂ in ten healthy volunteers.
(cont.) QUIXOTIC-measured CMRO₂ is found to be within the expected physiological range and is comparable to values reported by other techniques. QUIXOTIC is then applied to evaluate CMRO₂ response to carbon-dioxide-induced hypercapnia in awake humans. In this study, CMRO₂ is observed to decrease in response to mild hypercapnia. Finally, pilot studies that show feasibility of QUIXOTIC-based functional MRI (fMRI) and so-called "turbo" QUIXOTIC are presented and discussed.
by Divya Sanam Bolar.
Ph.D.
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Tan, Hsueh-Li. « The Role of Tomato Bioactive Components and CMO2 Gene Interaction in Prostate Cancer Prevention ». The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1345493048.

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ZENATTI, MURIEL. « Des raisons biochimiques de l'atteinte preferentielle de la corticosterone methyl oxydase de type 2 (cmo2) dans le carcinome surrenalien ». Paris 6, 1993. http://www.theses.fr/1993PA066281.

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Afin de demontrer que les carcinomes surrenaliens etudies presentent des anomalies de l'hormonosynthese au niveau de la voie de l'aldosterone, et de tenter de comprendre comment et pourquoi il en est ainsi, differentes voies d'approche ont ete utilisees. Les taux plasmatiques de 11-desoxycorticosterone, 18-hydroxy-11desoxycorticosterone, corticosterone (b), 18-hydroxycorticosterone (18-ohb) et aldosterone ont tous ete determines par dosage radioimmunologique precede d'une etape de separation chromatographique, chez 21 patients presentant differents types de tumeurs surrenaliennes identifiees sur des criteres histologiques (12 carcinomes dont 5 metastatiques, 7 adenomes, 1 hyperplasie, 1 metastase de cancer colique). Les resultats montrent que dans tous les cas de carcinomes surrenaliens etudies ici, on observe la coexistence constante d'un hypoaldosteronisme contrastant avec des taux plasmatiques variables mais non effondres des precurseurs de l'aldosterone. La mise en evidence par des travaux de genetique d'un defaut d'expression du gene cyp11b2 dans un cas de carcinome surrenalien metastatique (alors que celle du gene cyp11b1 n'est pas modifiee par rapport a la surrenale humaine normale) confirment les resultats de l'exploration biologique et permettent de localiser le dysfonctionnement de la voie de synthese de l'aldosterone observe au niveau de l'activite corticosterone methyl oxydase de type 2 (cmo2) de l'aldosynthase. Une etude in vitro par incubation de mitochondries de surrenales de canard en presence de b ou de 18 ohb tritiee et de l malate a mis en evidence la labilite preferentielle intrinseque de l'activite cmo2 de l'aldosynthase, qui peut etre mise en relation avec une difference de liaison de la b et de la 18-ohb au cytochrome p450 catalysant ces reactions. En conclusion, en depit du nombre limite de cas, l'ensemble des resultats suggere que les carcinomes surrenaliens presentent des anomalies de l'hormonosynthese se traduisant sur la voie des mineralocorticoides par un dysfonctionnement de l'aldosynthase au niveau de son activite cmo2 qui, compte tenu de sa labilite preferentielle intrinseque, doit etre atteinte precocement lors du developpement d'un processus tumoral malin de la surrenale
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Chapitres de livres sur le sujet "CMRO2"

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Bale, Gemma, Ajay Rajaram, Matthew Kewin, Laura Morrison, Alan Bainbridge, Linshan Liu, Udunna Anazodo, Mamadou Diop, Keith St Lawrence et Ilias Tachtsidis. « Multimodal Measurements of Brain Tissue Metabolism and Perfusion in a Neonatal Model of Hypoxic-Ischaemic Injury ». Dans Advances in Experimental Medicine and Biology, 203–8. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-48238-1_32.

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AbstractThis is the first multimodal study of cerebral tissue metabolism and perfusion post-hypoxic-ischaemic (HI) brain injury using broadband near-infrared spectroscopy (bNIRS), diffuse correlation spectroscopy (DCS), positron emission tomography (PET) and magnetic resonance spectroscopy (MRS). In seven piglet preclinical models of neonatal HI, we measured cerebral tissue saturation (StO2), cerebral blood flow (CBF), cerebral oxygen metabolism (CMRO2), changes in the mitochondrial oxidation state of cytochrome c oxidase (oxCCO), cerebral glucose metabolism (CMRglc) and tissue biochemistry (Lac+Thr/tNAA). At baseline, the parameters measured in the piglets that experience HI (not controls) were 64 ± 6% StO2, 35 ± 11 ml/100 g/min CBF and 2.0 ± 0.4 μmol/100 g/min CMRO2. After HI, the parameters measured were 68 ± 6% StO2, 35 ± 6 ml/100 g/min CBF, 1.3 ± 0.1 μmol/100 g/min CMRO2, 0.4 ± 0.2 Lac+Thr/tNAA and 9.5 ± 2.0 CMRglc. This study demonstrates the capacity of a multimodal set-up to interrogate the pathophysiology of HIE using a combination of optical methods, MRS, and PET.
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Hyder, Fahmeed, et Hal Blumenfeld. « Relationship between CMRO2 and Neuronal Activity ». Dans Brain Energetics and Neuronal Activity, 173–94. Chichester, UK : John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470020520.ch10.

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Hyder, Fahmeed. « Deriving Changes in CMRO2 from Calibrated fMRI ». Dans Brain Energetics and Neuronal Activity, 147–71. Chichester, UK : John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470020520.ch9.

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Smith, David S. « Drug Induced Depression of CMRO2 During Aneurysm Clipping ». Dans Anesthesia and the Central Nervous System, 329–40. Dordrecht : Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1610-7_27.

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Klementavicius, R., E. M. Nemoto et H. Yonas. « Basal Q10 for Cerebral Metabolic Rate for Oxygen (CMRO2) in Rats ». Dans Advances in Experimental Medicine and Biology, 191–95. Boston, MA : Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0333-6_23.

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Chen, Wei, Xiao-Hong Zhu et Kamil Ugurbil. « Imaging Cerebral Metabolic Rate of Oxygen Consumption (CMRO2) Using 17O NMR Approach at Ultrahigh Field ». Dans Brain Energetics and Neuronal Activity, 125–46. Chichester, UK : John Wiley & Sons, Ltd, 2005. http://dx.doi.org/10.1002/0470020520.ch8.

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Nemoto, Edwin M., John A. Melick et Peter Winter. « Active and Basal Cerebrometabolic Rate for Oxygen (CMRO2) After Complete Global Brain Ischemia in Rats ». Dans Oxygen Transport to Tissue X, 391–96. New York, NY : Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9510-6_46.

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Nemoto, Edwin M., Richard Klementavicius et Howard Yonas. « Functional and Basal Cerebral Metabolic Rate for Oxygen (CMRO2) and its Relevance to the Pathogenesis and Therapy of Brain Injury ». Dans Oxygen Transport to Tissue XX, 235–42. Boston, MA : Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4863-8_28.

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« CMRO2 Mapping by Calibrated fMRI ». Dans Quantifying Morphology and Physiology of the Human Body Using MRI, 99–124. CRC Press, 2013. http://dx.doi.org/10.1201/b14814-8.

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« Mean cerebral blood flow (m-CBF) and cerebral oxygen utilization (CMRO2) in patients with ruptured intracranial aneurysm in the acute stage ». Dans Timing of Aneurysm Surgery, 61–70. De Gruyter, 1985. http://dx.doi.org/10.1515/9783110858853-010.

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Actes de conférences sur le sujet "CMRO2"

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Allen, M. S., T. J. Huppert et D. A. Boas. « Estimating CMRO2 with multi-modality imaging using a multi-compartment vascular model ». Dans Biomedical Topical Meeting. Washington, D.C. : OSA, 2006. http://dx.doi.org/10.1364/bio.2006.tuc9.

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Sakadžić, Sava, Mohammad A. Yaseen, Rajeshwer S. Jaswal, Emmanuel Roussakis, Anders M. Dale, Richard B. Buxton, Sergei A. Vinogradov, David A. Boas et Anna Devor. « Two-photon microscopy measurement of CMRO2 using periarteriolar PO2 gradients (Conference Presentation) ». Dans Neural Imaging and Sensing, sous la direction de Qingming Luo et Jun Ding. SPIE, 2017. http://dx.doi.org/10.1117/12.2253690.

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Gagnon, Louis, Sava Sakadžić, Frédéric Lesage, Philippe Pouliot, Anders M. Dale, Anna Devor, Richard B. Buxton et David A. Boas. « Improving the calibrated fMRI estimation of CMRO2 with oxygen-sensitive Two-Photon Microscopy ». Dans Cancer Imaging and Therapy. Washington, D.C. : OSA, 2016. http://dx.doi.org/10.1364/cancer.2016.jw3a.18.

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Chong, Sang Hoon, Yi Hong Ong, Mirna El Khatib, Srinivasa Rao Allu, Ashwin B. Parthasarathy, Joel H. Greenberg, Arjun G. Yodh et Sergei A. Vinogradov. « Real-time measurements of pO2 gradients, CBF, and CMRO2 in the rat brain during functional activation ». Dans Neural Imaging and Sensing 2021, sous la direction de Qingming Luo, Jun Ding et Ling Fu. SPIE, 2021. http://dx.doi.org/10.1117/12.2579418.

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Yaseen, Mohammad A., Vivek J. Srinivasan, Sava Sakadžić, Sergei A. Vinogradov et David A. Boas. « Optically based quantification of absolute cerebral metabolic rate of oxygen (CMRO2) with high spatial resolution in rodents ». Dans BiOS, sous la direction de Nikiforos Kollias, Bernard Choi, Haishan Zeng, Reza S. Malek, Brian J. Wong, Justus F. R. Ilgner, Kenton W. Gregory et al. SPIE, 2010. http://dx.doi.org/10.1117/12.842904.

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Fischer, A. J., D. D. Koleske et J. R. Wendt. « Surface plasmon enhanced emission from InGaN single-quantum-well light emitting diodes ». Dans Conference on Lasers and Electro-Optics. Washington, D.C. : OSA, 2009. http://dx.doi.org/10.1364/cleo.2009.cmoo2.

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Mutter, Lukas, Vladimir Iakovlev, Andrei Caliman, Alexandru Mereuta, Alexei Sirbu et Eli Kapon. « 1.3-µm Wavelength Coupled VCSEL Arrays Employing Patterned Tunnel Junction ». Dans Conference on Lasers and Electro-Optics. Washington, D.C. : OSA, 2009. http://dx.doi.org/10.1364/cleo.2009.cmrr2.

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Klotzkin, David, Peter G. Goetz, William S. Rabinovich, Mike S. Ferraro, Rita Mahon et Steven C. Binari. « Integrated Angle-of-Arrival Sensing and Simultaneous Bidirectional Communication Using a Cat’s eye Modulating Retroreflector ». Dans Conference on Lasers and Electro-Optics. Washington, D.C. : OSA, 2009. http://dx.doi.org/10.1364/cleo.2009.cmo2.

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Tsai, Meng-Tsan, Cheng-Kuang Lee, Hsiang-Chieh Lee, Yih-Ming Wang, C. C. Yang et Chun-Pin Chiang. « Effective Indicators for Oral Cancer Diagnosis Based on Optical Coherence Tomography ». Dans Conference on Lasers and Electro-Optics. Washington, D.C. : OSA, 2009. http://dx.doi.org/10.1364/cleo.2009.cmr2.

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Tan, Meng Peun, Ansas M. Kasten, Dominic F. Siriani, Joshua D. Sulkin et Kent D. Choquette. « Proton-Implanted 850-nm Photonic Crystal Vertical-Cavity Surface-Emitting Lasers with Improved Performance ». Dans Conference on Lasers and Electro-Optics. Washington, D.C. : OSA, 2010. http://dx.doi.org/10.1364/cleo.2010.cmo2.

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