Examining Linguistic Behavior of a Virtual Museum Guide

As artificial intelligence that uses natural language processing becomes more prevalent, analyzing such software so that it maximally understands us holds all the more significance. Despite the high accuracy at which recurrent neural networks can predict, say, the next word in a sentence, they function differently than a human brain. Given that the sources of difficulty encountered by a natural language processing software may not be intuitive to a human, searching for patterns among its errors provides insight as to where software can be improved. Additionally, given that language is productive, humans interacting with natural language processing technology can produce an unlimited variety of stimuli. When a stimulus is as unpredictable as a human prompted to ask whatever they want, the response it yields reveals how natural language processing software handles variability. At the Center of Science and Industry (COSI), a science museum in Columbus, Ohio, researchers from the Ohio State University have developed an interactive avatar that uses natural language processing. In this context, an avatar can be defined as a human-like bot created to interact with users. Visitors can ask the avatar questions related to linguistics, computer science, and exhibits at the museum. The avatar consists of both an animated visual component and its artificial intelligence software, which processes speech as input and produces a response accordingly. In this case, the artificial intelligence used to process language is a recurrent neural network, pretrained on a large corpus of general English text, then subsequently trained on a smaller corpus of text pertaining to computer science, linguistics, and COSI exhibits. My research focuses on the effectiveness of the avatar's responses.No embargoAcademic Major: Linguistic

Longitudinal transcriptomic analysis of mouse sciatic nerve reveals pathways associated with age‐related muscle pathology

Abstract Background Sarcopenia, the age‐associated decline in skeletal muscle mass and strength, has long been considered a disease of muscle only, but accumulating evidence suggests that sarcopenia could originate from the neural components controlling muscles. To identify early molecular changes in nerves that may drive sarcopenia initiation, we performed a longitudinal transcriptomic analysis of the sciatic nerve, which governs lower limb muscles, in aging mice. Methods Sciatic nerve and gastrocnemius muscle were obtained from female C57BL/6JN mice aged 5, 18, 21 and 24 months old (n = 6 per age group). Sciatic nerve RNA was extracted and underwent RNA sequencing (RNA‐seq). Differentially expressed genes (DEGs) were validated using quantitative reverse transcription PCR (qRT‐PCR). Functional enrichment analysis of clusters of genes associated with patterns of gene expression across age groups (adjusted P‐value  2; false discovery rate [FDR] < 0.05). Up‐regulated DEGs included Dbp (log2 fold change [LFC] = 2.63, FDR < 0.001) and Lmod2 (LFC = 7.52, FDR = 0.001). Down‐regulated DEGs included Cdh6 (LFC = −21.38, FDR < 0.001) and Gbp1 (LFC = −21.78, FDR < 0.001). We validated RNA‐seq findings with qRT‐PCR of various up‐ and down‐regulated genes including Dbp and Cdh6. Up‐regulated genes (FDR < 0.1) were associated with the AMP‐activated protein kinase signalling pathway (FDR = 0.02) and circadian rhythm (FDR = 0.02), whereas down‐regulated DEGs were associated with biosynthesis and metabolic pathways (FDR < 0.05). We identified seven significant clusters of genes (FDR < 0.05, LRT) with similar expression patterns across groups. Functional enrichment analysis of these clusters revealed biological processes that may be implicated in age‐related changes in skeletal muscles and/or sarcopenia initiation including extracellular matrix organization and an immune response (FDR < 0.05). Conclusions Gene expression changes in mouse peripheral nerve were detected prior to disturbances in myofiber innervation and sarcopenia onset. These early molecular changes we report shed a new light on biological processes that may be implicated in sarcopenia initiation and pathogenesis. Future studies are warranted to confirm the disease modifying and/or biomarker potential of the key changes we report here