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1 s to examine brain changes that characterize acute intoxication.
2 n species (ROS) formation, such as in H(2) S acute intoxication.
3 uding the development of hyperthermia during acute intoxication.
5 nephrotoxicity in the absence of episodes of acute intoxication and that duration of therapy and cumu
6 ally dosed to overcome tolerance and achieve acute intoxication) and identical placebo, randomized fo
7 en associated with impaired cognition during acute intoxication as well as in the unintoxicated state
8 r the formation of *CO(2)(-) radicals during acute intoxication by sodium formate, suggesting a free
9 flies exposed to cocaine display features of acute intoxication like those observed in mammals, inclu
10 nabis regularly, to determine the effects of acute intoxication on prefrontal cortex resting-state me
11 ars prior to the interview, which eliminates acute intoxication or withdrawal effects as an explanati
14 ear mortality (1382 [31.2%]) relative to the acute intoxication subgroup (42 [4.0%]) (adjusted hazard
15 gradient from low-frequency service use for acute intoxication to high-frequency service use for sev
16 nol-related behaviors in flies, ranging from acute intoxication to self-administration and reward, ha
17 In a rat model of pneumonia, the effects of acute intoxication were monitored for lung chemokine res
19 Children were the most exposed population to acute intoxication with HT-2 toxin in conventional pista
20 rial function and reduce brain injury during acute intoxication with the OP diisopropylfluorophosphat
21 Psychomotor function is most affected during acute intoxication, with some evidence for persistence i