Iowa State University

About: Iowa State University is a education organization based out in Ames, Iowa, United States. It is known for research contribution in the topics: Population & Gene. The organization has 50151 authors who have published 107716 publications receiving 3355909 citations. The organization is also known as: Iowa State University of Science and Technology & Iowa State College.

Stabilization of linear systems with limited information

Abstract: We show that the coarsest, or least dense, quantizer that quadratically stabilizes a single input linear discrete time invariant system is logarithmic, and can be computed by solving a special linear quadratic regulator problem. We provide a closed form for the optimal logarithmic base exclusively in terms of the unstable eigenvalues of the system. We show how to design quantized state-feedback controllers, and quantized state estimators. This leads to the design of hybrid output feedback controllers. The theory is then extended to sampling and quantization of continuous time linear systems sampled at constant time intervals. We generalize the definition of density of quantization to the density of sampling and quantization in a natural way, and search for the coarsest sampling and quantization scheme that ensures stability. Finally, by relaxing the definition of quadratic stability, we show how to construct logarithmic quantizers with only finite number of quantization levels and still achieve practical stability of the closed-loop system.

Threatened egotism, narcissism, self-esteem, and direct and displaced aggression: Does self-love or self-hate lead to violence?

Abstract: It has been widely asserted that low self-esteem causes violence, but laboratory evidence is lacking, and some contrary observations have characterized aggressors as having favorable self-opinions. In 2 studies, both simple self-esteem and narcissism were measured, and then individual participants were given an opportunity to aggress against someone who had insulted them or praised them or against an innocent third person. Self-esteem proved irrelevant to aggression. The combination of narcissism and insult led to exceptionally high levels of aggression toward the source of the insult. Neither form of self-regard affected displaced aggression, which was low in general. These findings contradict the popular view that low self-esteem causes aggression and point instead toward threatened egotism as an important cause.

Violent Video Game Effects on Aggression, Empathy, and Prosocial Behavior in Eastern and Western Countries: A Meta-Analytic Review.

Abstract: Meta-analytic procedures were used to test the effects of violent video games on aggressive behavior, aggressive cognition, aggressive affect, physiological arousal, empathy/desensitization, and prosocial behavior. Unique features of this meta-analytic review include (a) more restrictive methodological quality inclusion criteria than in past meta-analyses; (b) cross-cultural comparisons; (c) longitudinal studies for all outcomes except physiological arousal; (d) conservative statistical controls; (e) multiple moderator analyses; and (f) sensitivity analyses. Social-cognitive models and cultural differences between Japan and Western countries were used to generate theory-based predictions. Meta-analyses yielded significant effects for all 6 outcome variables. The pattern of results for different outcomes and research designs (experimental, cross-sectional, longitudinal) fit theoretical predictions well. The evidence strongly suggests that exposure to violent video games is a causal risk factor for increased aggressive behavior, aggressive cognition, and aggressive affect and for decreased empathy and prosocial behavior. Moderator analyses revealed significant research design effects, weak evidence of cultural differences in susceptibility and type of measurement effects, and no evidence of sex differences in susceptibility. Results of various sensitivity analyses revealed these effects to be robust, with little evidence of selection (publication) bias.

The continuation power flow: a tool for steady state voltage stability analysis

Abstract: The authors present a method of finding a continuum of power flow solutions starting at some base load and leading to the steady-state voltage stability limit (critical point) of the system. A salient feature of the so-called continuation power flow is that it remains well-conditioned at and around the critical point. As a consequence, divergence due to ill-conditioning is not encountered at the critical point, even when single-precision computation is used. Intermediate results of the process are used to develop a voltage stability index and identify areas of the system most prone to voltage collapse. Examples are given where the voltage stability of a system is analyzed using several different scenarios of load increase. >

Glutamate-mediated astrocyte-neuron signalling.

Abstract: NEUROTRANSMITTER released from neurons is known to signal to neighbouring neurons and glia1–3 Here we demonstrate an additional signalling pathway in which glutamate is released from astrocytes and causes an NMDA (N-methyl-d-aspartate) receptor-mediated increase in neuronal calcium. Internal calcium was elevated and glutamate release stimulated by application of the neuro-ligand bradykinin to cultured astrocytes. Elevation of astrocyte internal calcium was also sufficient to induce glutamate release. To determine whether this released glutamate signals to neurons, we studied astrocyte–neuron co-cultures. Bradykinin significantly increased calcium levels in neurons co-cultured with astrocytes, but not in solitary neurons. The glutamate receptor antagonists d-2-amino-5-phosphonopentanoic acid and d-glutamylglycine prevented bradykinin-induced neuronal calcium elevation. When single astrocytes were directly stimulated to increase internal calcium and release glutamate, calcium levels of adjacent neurons were increased; this increase could be blocked by d-glutamylglycine. Thus, astrocytes regulate neuronal calcium levels through the calcium-dependent release of glutamate.