Learning Dialogue Strategies from Older and Younger Simulated Users

Older adults are a challenging user group because their behaviour can be highly variable. To the best of our knowledge, this is the first study where dialogue strategies are learned and evaluated with both simulated younger users and simulated older users. The simulated users were derived from a corpus of interactions with a strict system-initiative spoken dialogue system (SDS). Learning from simulated younger users leads to a policy which is close to one of the dialogue strategies of the underlying SDS, while the simulated older users allow us to learn more flexible dialogue strategies that accommodate mixed initiative. We conclude that simulated users are a useful technique for modelling the behaviour of new user groups

Being Old Doesn't Mean Acting Old: How Older Users Interact with Spoken Dialogue System.

Most studies on adapting voice interfaces to older users work top-down by comparing the interaction behavior of older and younger users. In contrast, we present a bottom-up approach. A statistical cluster analysis of 447 appointment scheduling dialogs between 50 older and younger users and 9 simulated spoken dialog systems revealed two main user groups, a “social” group and a “factual” group. “Factual” users adapted quickly to the systems and interacted efficiently with them. “Social” users, on the other hand, were more likely to treat the system like a human, and did not adapt their interaction style. While almost all “social” users were older, over a third of all older users belonged in the “factual” group. Cognitive abilities and gender did not predict group membership. We conclude that spoken dialog systems should adapt to users based on observed behavior, not on age

The MATCH Corpus: A Corpus of Older and Younger Users' Interactions With Spoken Dialogue Systems.

We present the MATCH corpus, a unique data set of 447 dialogues in which 26 older and 24 younger adults interact with nine different spoken dialogue systems. The systems varied in the number of options presented and the confirmation strategy used. The corpus also contains information about the users’ cognitive abilities and detailed usability assessments of each dialogue system. The corpus, which was collected using a Wizard-of-Oz methodology, has been fully transcribed and annotated with dialogue acts and ‘‘Information State Update’’ (ISU) representations of dialogue context. Dialogue act and ISU annotations were performed semi-automatically. In addition to describing the corpus collection and annotation, we present a quantitative analysis of the interaction behaviour of older and younger users and discuss further applications of the corpus. We expect that the corpus will provide a key resource for modelling older people’s interaction with spoken dialogue systems

mTORC1-dependent protein synthesis and autophagy uncouple in the regulation of Apolipoprotein A-I expression

Background: Apolipoprotein A-I (ApoA-I) is involved in reverse cholesterol transport as a major component of HDL, but also conveys anti-thrombotic, anti-oxidative, anti-inflammatory and immune-regulatory properties that are pertinent to its protective roles in cardiovascular, inflammatory and malignant pathologies. Despite the pleiotropy in ApoA-I functions, the regulation of intracellular ApoA-I levels remains poorly explored. Methods: HepG2 hepatoma cells and primary mouse hepatocytes were used as in vitro models to study the impact of genetic and chemical inhibitors of autophagy and the proteasome on ApoA-I by immunoblot, immunofluorescence and electron microscopy. Different growth conditions were implemented in conjunction with mTORC inhibitors to model the influence of nutrient scarcity versus sufficiency on ApoA-I regulation. Hepatic ApoA-I expression was also evaluated in high fat diet-fed mice displaying blockade in autophagy. Results: Under nutrient-rich conditions, basal ApoA-I levels in liver cells are sustained by the balancing act of autophagy and of mTORC1-dependent de novo protein synthesis. ApoA-I proteolysis occurs through a canonical autophagic pathway involving Beclin1 and ULK1 and the receptor protein p62/SQSTM1 that targets ApoA-I to autophagosomes. However, upon aminoacid insufficiency, suppression of ApoA-I synthesis prevails, rendering mTORC1 inactivation dispensable for autophagy-mediated ApoA-I proteolysis. Conclusion: These data underscore the major contribution of post-transcriptional mechanisms to ApoA-I levels which differentially involve mTORC1-dependent signaling to protein synthesis and autophagy, depending on nutrient availability. Given the established role of ApoA-I in HDL-mediated reverse cholesterol transport, this mode of ApoA-I regulation may reflect a hepatocellular response to the organismal requirement for maintenance of cholesterol and lipid reserves under conditions of nutrient scarcity. © 2020 Elsevier Inc

Cell adhesion tunes inflammatory TPL2 kinase signal transduction

Signaling through adhesion-related molecules is important for cancer growth and metastasis and cancer cells are resistant to anoikis, a form of cell death ensued by cell detachment from the extracellular matrix. Herein, we report that detached carcinoma cells and immortalized fibroblasts display defects in TNF and CD40 ligand (CD40L)-induced MEK-ERK signaling. Cell detachment results in reduced basal levels of the MEK kinase TPL2, compromises TPL2 activation and sensitizes carcinoma cells to death-inducing receptor ligands, mimicking the synthetic lethal interactions between TPL2 inactivation and TNF or CD40L stimulation. Focal Adhesion Kinase (FAK), which is activated in focal adhesions and mediates anchorage-dependent survival signaling, was found to sustain steady state TPL2 protein levels and to be required for TNF-induced TPL2 signal transduction. We show that when FAK levels are reduced, as seen in certain types of malignancy or malignant cell populations, the formation of cIAP2:RIPK1 complexes increases, leading to reduced TPL2 expression levels by a dual mechanism: first, by the reduction in the levels of NF-κΒ1 which is required for TPL2 stability; second, by the engagement of an RelA NF-κΒ pathway that elevates interleukin-6 production, leading to activation of STAT3 and its transcriptional target SKP2 which functions as a TPL2 E3 ubiquitin ligase. These data underscore a new mode of regulation of TNF family signal transduction on the TPL2-MEK-ERK branch by adhesion-related molecules that may have important ramifications for cancer therapy. © 2022, The Author(s), under exclusive licence to Springer Nature Switzerland AG

AN INTEGRATED SYSTEM FOR SMART-HOME CONTROL OF APPLIANCES BASED ON REMOTE SPEECH INTERACTION

We present an integrated system that uses speech as a natural input modality to provide user-friendly access to information and entertainment devices installed in a real home environment. The system is based on a combination of beamforming techniques and speech recognition. The general problem addressed in this work is that of hands-free speech recognition in a reverberant room where users walk while engaged in conversation in the presence of different types of house-specific noisy conditions (e.g. TV/radio broadcast, interfering speakers, ventilator/air-condition noise, etc). The paper focuses on implementation details and practical considerations concerning the integration of diverse technologies into a working system. 1