Système prototype pour le suivi des changements de l'occupation du sol en milieu urbain fondé sur les images du satellite RADARSAT-1

Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal

General anesthesia, sleep and coma

In the United States, nearly 60,000 patients per day receive general anesthesia for surgery.1 General anesthesia is a drug-induced, reversible condition that includes specific behavioral and physiological traits — unconsciousness, amnesia, analgesia, and akinesia — with concomitant stability of the autonomic, cardiovascular, respiratory, and thermoregulatory systems.2 General anesthesia produces distinct patterns on the electroencephalogram (EEG), the most common of which is a progressive increase in low-frequency, high-amplitude activity as the level of general anesthesia deepens3,4 (Figure 1Figure 1Electroencephalographic (EEG) Patterns during the Awake State, General Anesthesia, and Sleep.). How anesthetic drugs induce and maintain the behavioral states of general anesthesia is an important question in medicine and neuroscience.6 Substantial insights can be gained by considering the relationship of general anesthesia to sleep and to coma. Humans spend approximately one third of their lives asleep. Sleep, a state of decreased arousal that is actively generated by nuclei in the hypothalamus, brain stem, and basal forebrain, is crucial for the maintenance of health.7,8 Normal human sleep cycles between two states — rapid-eye-movement (REM) sleep and non-REM sleep — at approximately 90-minute intervals. REM sleep is characterized by rapid eye movements, dreaming, irregularities of respiration and heart rate, penile and clitoral erection, and airway and skeletal-muscle hypotonia.7 In REM sleep, the EEG shows active high-frequency, low-amplitude rhythms (Figure 1). Non-REM sleep has three distinct EEG stages, with higher-amplitude, lower-frequency rhythms accompanied by waxing and waning muscle tone, decreased body temperature, and decreased heart rate. Coma is a state of profound unresponsiveness, usually the result of a severe brain injury.9 Comatose patients typically lie with eyes closed and cannot be roused to respond appropriately to vigorous stimulation. A comatose patient may grimace, move limbs, and have stereotypical withdrawal responses to painful stimuli yet make no localizing responses or discrete defensive movements. As the coma deepens, the patient's responsiveness even to painful stimuli may diminish or disappear. Although the patterns of EEG activity observed in comatose patients depend on the extent of the brain injury, they frequently resemble the high–amplitude, low-frequency activity seen in patients under general anesthesia10 (Figure 1). General anesthesia is, in fact, a reversible drug-induced coma. Nevertheless, anesthesiologists refer to it as “sleep” to avoid disquieting patients. Unfortunately, anesthesiologists also use the word “sleep” in technical descriptions to refer to unconsciousness induced by anesthetic drugs.11 (For a glossary of terms commonly used in the field of anesthesiology, see the Supplementary Appendix, available with the full text of this article at NEJM.org.) This review discusses the clinical and neurophysiological features of general anesthesia and their relationships to sleep and coma, focusing on the neural mechanisms of unconsciousness induced by selected intravenous anesthetic drugs.Massachusetts General Hospital. Dept. of Anesthesia and Critical Care, and Pain MedicineNational Institutes of Health (NIH) (Director’s Pioneer Award DP1OD003646)University of Michigan. Dept. of AnesthesiologyNational Institutes of Health (U.S.) (grant HL40881)National Institutes of Health (U.S.) (grant HL65272)James S. McDonnell FoundationNational Institutes of Health (U.S.) (grant HD51912

An automatic road extraction method using a map-guided approachcombined with neural networks for cartographic database validation purposes

International audienceA method is proposed to extract road intersections from a SPOT panchromatic image, using a map-guided approach combined with the application of a neural network. The results show an average increase of 36% of planimetric accuracy after applying the method instead of simply superimposing the roads on the geocoded image. Also, only 8 out 42 samples were previously correctly traced, compared to 27 after application of the algorithm

Map-image matching using a multi-layer perceptron : the case of the road network

International audienc

T-tubule localization of the inward-rectifier K+ channel in mouse ventricular myocytes: a role in K+ accumulation

The properties of the slow inward ‘tail currents’ (Itail) that followed depolarizing steps in voltage-clamped, isolated mouse ventricular myocytes were examined. Depolarizing steps that produced large outward K+ currents in these myocytes were followed by a slowly decaying inward Itail on repolarization to the holding potential. These currents were produced only by depolarizations: inwardly rectifying K+ currents, IK1, produced by steps to potentials negative to the holding potential, were not followed by Itail.For depolarizations of equal duration, the magnitude of Itail increased as the magnitude of outward current at the end of the depolarizing step increased. The apparent reversal potential of Itail was dependent upon the duration of the depolarizing step, and the reversal potential shifted to more depolarized potentials as the duration of the depolarization was increased.Removal of external Na+ and Ca2+ had no significant effect on the magnitude or time course of Itail. BaCl2 (0.25 mm), which had no effect on the magnitude of outward currents, abolished Itail and IK1 simultaneously.Accordingly, Itail in mouse ventricular myocytes probably results from K+ accumulation in a restricted extracellular space such as the transverse tubule system (t-tubules). The efflux of K+ into the t-tubules during outward currents produced by depolarization shifts the K+ Nernst potential (EK) from its ‘resting’ value (close to −80 mV) to more depolarized potentials. This suggests that Itail is produced by IK1 in the t-tubules and is inward because of the transiently elevated K+ concentration and depolarized value of EK in the t-tubules.Additional evidence for the localization of IK1 channels in the t-tubules was provided by confocal microscopy using a specific antibody against Kir2.1 in mouse ventricular myocytes

COMPUTER GAMES AS HOMEWORK: How to delight and instruct

We are interested in exploring how entertainment in games can be combined with educational goals to make a compelling experience. In this paper we present our design study for the development of a mod game, Antarctic NWN. We first present the background for the game, objectives, and then discuss the gameplay o f Antarctic NWN. We then explore issues that influence the design of a gripping game. One important issue is the relation between reality, simulation and game word. Then we focus on enhancing emotional involvement. Emotion is especially relevant to role-play game as it draws players into the story, and supports aesthetic understanding. We also look more specifically at the role of humour in this context. Humour enhanceslearning as well as providing a more pleasurable experience. In our quest to understand how games can both delight and instruct, we review the environment in which our game might be played, within the classroom or as family entertainment and describe different scenarios of use

Enhancement of the signal-to-noise ratio in (H2O)-O-15 bolus PET activation images: A combined cold-bolus, switched protocol

To increase the signal-to-noise ratio (S/N) of (H2O)-O-15 bolus PET activation images, we designed and tested a data acquisition protocol that alters the relative distribution of tracer in the uptake and washout phases of the input function. This protocol enhances the S/N gains obtained with conventional switched protocols by combining task switching and the use of a large bolus of blood free of tracer (cold bolus). The cold bolus is formed by sequestering blood in the lower limbs with a double cuff before tracer injection. Methods: The effect of a combined cold-bolus, switched protocol on the signal from activation images was first simulated using a compartmental model of the uptake of (H2O)-O-15 into the brain. Then, the effectiveness of the protocol was investigated in 4 healthy volunteers performing a language task. Each volunteer underwent scanning 12 times: 3 activation/baseline and 3 baseline/activation scans using the conventional switched protocol and 3 activation/baseline and 3 baseline/activation scans using the combined cold-bolus, switched protocol. The S/N changes introduced when using the cold bolus were analyzed by comparing, across protocols, the magnitude and statistical significance of the activation foci associated with the execution of the language task identified in the averaged subtracted images, and by comparing image noise levels. Results: In the simulated datasets, the combined protocol yielded a substantial increase in the activation signals for scan durations greater than 60 s, in comparison with equivalent signals yielded by the switched protocol alone. In the PET experiments, activation foci obtained using the combined protocol had significantly higher t statistic values than did equivalent foci detected using the conventional switched protocol (mean improvement, 36%). Analysis of the S/N in the averaged subtracted images revealed that the improvements in statistical significance of the activation foci were caused by increases in the signal magnitudes and not by decreases in overall image noise. Conclusion: We designed a data acquisition protocol for (H2O)-O-15 bolus PET activation studies that combines the use of a tracer-free bolus with a switched protocol. Simulated and experimental data suggest that this combined protocol enhances the S/N gains obtained with a conventional switched protocol. Implementation of the combined protocol in (H2O)-O-15 bolus activation studies was easy