The goal of this project is to develop a pedestrian mobility aid for the elderly. In order for this type of assistive technology to be useful and accepted by its intended user community, it must enhance the abilities of users, not replace them. This leads to an agent architecture in which the agent must operate without hindering the user's ability to take direct action when they choose. In other words, the agent cannot simply be a proxy for the user's actions. The agent must select its own goals based on observations of its user's actions. This is crucial not only because users may have diminished capacity to explain their actions to an agent, but because the ability of the agent to correctly interpret the user's goals is tied to its ability to act while still allowing the user to "feel in control". We present a mobility aid, i.e. a wheeled walker, which varies its goals and level of activity based on an estimation of its user's intentions. The assistive agent often takes no action, allowing the user to be fully in control. When the ease or safety of the user's travel is threatened, the agent attempts to influence the user's motion based on its belief in the user's goal. By varying the degree of autonomy, the walker can adjust to the user as their abilities change from day to day, or hour to hour. This prevents the walker from "trying to do too much", allowing the user to feel as if they are in control and not being "lead".
Since its discovery in the early 1980s, there has been significant progress in understanding the biology of type 1 human immunodeficiency virus (HIV-1). Structural biologists have made tremendous contributions to this challenge, guiding the development of current therapeutic strategies. Despite our efforts, there are unresolved structural features of the virus and consequently, significant knowledge gaps in our understanding. The superstructure of the HIV-1 matrix (MA) shell has not been elucidated. Evidence by various high-resolution microscopy techniques support a model composed of MA trimers arranged in a hexameric configuration consisting of 6 MA trimers forming a hexagon. In this manuscript we review the mathematical limitations of this model and propose a new model consisting of a 6-lune hosohedra structure, which aligns with available structural evidence. We used geometric and rotational matrix computation methods to construct our model and predict a new mechanism for viral entry that explains the increase in particle size observed during CD4 receptor engagement and the most common HIV-1 ellipsoidal shapes observed in cryo-EM tomograms. A better understanding of the HIV-1 MA shell structure is a key step towards better models for viral assembly, maturation and entry. Our new model will facilitate efforts to improve understanding of the biology of HIV-1.
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