Avatar - a multi-sensory system for real time body position monitoring.

Virtual reality and computer assisted physical rehabilitation applications require an unobtrusive and inexpensive real time monitoring systems. Existing systems are usually complex and expensive and based on infrared monitoring. In this paper we propose Avatar, a hybrid system consisting of off-the-shelf components and sensors. Absolute positioning of a few reference points is determined using infrared diode on subject's body and a set of Wii Remotes as optical sensors. Individual body segments are monitored by intelligent inertial sensor nodes iSense. A network of inertial nodes is controlled by a master node that serves as a gateway for communication with a capture device. Each sensor features a 3D accelerometer and a 2 axis gyroscope. Avatar system is used for control of avatars in Virtual Reality applications, but could be used in a variety of augmented reality, gaming, and computer assisted physical rehabilitation applications.

Ethanol and spatial localization.

Water (Exp. 1) and radial maze (Exp. 2) tasks permitted an evaluation of the relative degree of impairment imposed by ethanol (0, 0.75, 1.5, and 2.0 g/kg) on cognitive mapping vs. cued place learning. The tasks did not require working memory. A strong tendency emerged for ethanol-treated rats to persist in cognitive mapping strategies after the strategies were no longer useful, but there was no indication of a mapping impairment per se. When performance deficits appeared, they were equivalent across mapping and cued place tasks and may have reflected motivational effects of ethanol. In most instances, neither mapping nor cued place tasks were difficult for ethanol-treated animals unless the tasks required abandoning one strategy for another. The tenacity of ethanol-treated rats to use cognitive mapping strategies, particularly rats receiving the highest dose, proved consistent and theoretically decisive. The behavioral invariance of ethanol-treated rats is not caused by a cognitive mapping deficit. Rather, mapping is another domain in which ethanol reduces flexibility.

Sampling behavior in the radial maze and operant chamber: role of the hippocampus and prefrontal area.

Rats were observed in the radial maze and in an operant setting where "errors" were, within limits, impossible to commit. Under these circumstances, the animals were free to seek information from the environment by varying their behavior, if they chose to do so, without penalty of nonreward. Rats with hippocampal, but not prefrontal or parietal damage, sampled fewer successive arm choices in the maze and exhibited a greatly reduced sensory analysis of the maze and its context. In operant chambers equipped with multiple levers, only hippocampal lesion narrowed the variety of interresponse intervals, which resulted in rhythmic responding. In contrast, the distribution of responses across the three response targets was not influenced by central nervous system injury. This pattern of information deprivation imposed by the hippocampal lesion parallels the profile of performance of such animals on more conventional tasks that depend on such information for optimal performance. Importantly, the sampling deficits were not direct outcomes of the hippocampal damage. Close scrutiny revealed that the rigidity developed over time, albeit quite rapidly. Thus the narrowed behavioral variation following hippocampectomy depends on some interactive component of task experience. We argue that reward is the other critical ingredient.

Environmental control of energy metabolism in rats.

Food availability was arranged so that episodes of feeding were separated by long periods of deprivation. Distinctly different contexts were associated with each condition. For other animals, relatively short periods of deprivation stood in contrast to relatively long opportunities to free-feed, and were also embedded in widely differing physical contexts. These temporal relationships among the conditions were adjusted to sharpen the saliency of each metabolic condition and thereby enhance its associability with the distinctive environment in which each occurred. To avoid the possibility of circadian entrainment, the feeding or deprivation episodes occurred at unpredictable times according to a variable-time schedule. Following several training cycles and an extended period of free-feeding in a neutral environment, the animals were reexposed to the various contexts and sacrificed for metabolite assays. The environment predictive of feeding elevated adipocyte lipoprotein lipase activity and lowered the levels of serum free fatty acids. The deprivation context boosted serum triglycerides and blood urea nitrogen. The conditioned responses were all of a compensatory nature: Feeding cues resulted in accelerated caloric deposition, deprivation cues elicited conditioned mobilization of stored energy. While protein catabolism and several indices of fat metabolism appear to be conditionable, no evidence of environmental control of glycemic responses was observed.

Inhibitory effect of cyclic adenosine 2',3'-monophosphate on leucine incorporation by L5178Y cells.

The specificity of the reported stimulation of protein synthesis affected by dibutyryl adenosine cyclic 3',5'-monophosphate in L5178Y cells was tested by assaying the effect of adenosine cyclic 2',3'-monophosphate. Protein synthesis was assayed as total acid precipitable 3H-leucine. Leucine incorporation was inhibited by adenosine cyclic 2',3'-monophosphate. Alone, and in combination with actinomycin, 2',3'-cAMP inhibited leucine incorporation more rapidly and to a greater degree than did actinomycin alone. Since a similar potentiating effect was not observed with cordycepin, the hypothesis has been suggested that adenosine cyclic 2',3'-monophosphate inhibits protein synthesis by interfering with some post transcriptional event, perhaps modification of existing RNA. The results further suggest that 2,3 cyclic AMP may be antagonistic of the effects of 3,5 cyclic AMP, and as such may be useful as an inhibitor of that nucleotide's action.