This paper describes technology and tools for intelligent human-computer interaction (IHCI) where human cognitive, perceptual, motor, and affective factors are modeled and used to adapt the H-C interface. IHCI emphasizes that human behavior encompasses both apparent human behavior and the hidden mental state behind behavioral performance. IHCI expands on the interpretation of human activities, known as W4 (what, where, when, who). While W4 only addresses the apparent perceptual aspect of human behavior, the W5+ technology for IHCI described in this paper addresses also the why and how questions, whose solution requires recognizing specific cognitive states. IHCI integrates parsing and interpretation of nonverbal information with a computational cognitive model of the user, which, in turn, feeds into processes that adapt the interface to enhance operator performance and provide for rational decision-making. The technology proposed is based on a general four-stage interactive framework, which moves from parsing the raw sensory-motor input, to interpreting the user's motions and emotions, to building an understanding of the user's current cognitive state. It then diagnoses various problems in the situation and adapts the interface appropriately. The interactive component of the system improves processing at each stage. Examples of perceptual, behavioral, and cognitive tools are described throughout the paper. Adaptive and intelligent HCI are important for novel applications of computing, including ubiquitous and human-centered computing.
Objective
Dexmedetomidine (DEX) exhibits neuroprotective effects as a multifunctional neuroprotective agent in numerous neurological disorders. However, in traumatic brain injury (TBI), the molecular mechanisms of these neuroprotective effects remain unclear. The present study investigated whether DEX, which has been reported to exert protective effects against TBI, could attenuate neuroinflammatory‐induced apoptosis and clarified the underlying mechanisms.
Methods
A weight‐drop model was established, and DEX was intraperitoneally injected 30 min after inducing TBI in rats. The water content in the brain tissue was measured. Terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling (TUNEL) assays were performed on histopathological tissue sections to evaluate neuronal apoptosis. Enzyme‐linked immunosorbent assay and PCR were applied to detect the levels of the inflammatory factors, TNF‐α, IL‐1β, IL‐6, and NF‐κB.
Results
TBI–challenged rats exhibited significant neuronal apoptosis, which was characterized via the wet‐to‐dry weight ratio, neurobehavioral functions, TUNEL assay results and the levels of cleaved caspase‐3, Bax upregulation and Bcl‐2, which were attenuated by DEX. Western blot, immunohistochemistry, and PCR results revealed that DEX promoted Nrf2 expression and upregulated expression of the Nrf2 downstream factors, HO‐1 and NQO‐1. Furthermore, DEX treatment markedly prevented the downregulation of inflammatory response factors, TNF‐α, IL‐1β and NF‐κB, and IL‐6.
Interpretation
Administering DEX attenuated inflammation‐induced brain injury in a TBI model, potentially via the Nrf2 signaling pathway.
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