Adaptation of the difficulty level in an infant-robot movement contingency study

19th International Workshop of Physical Agents (WAF). Madrid (22-23 Noviembre 2018)ABSTRACT: This paper presents a personalized contingency feedback adaptation system that aims to encourage infants aged 6 to 8 months to gradually increase the peak acceleration of their leg movements. The ultimate challenge is to determine if a socially assistive humanoid robot can guide infant learning using contingent rewards, where the reward threshold is personalized for each infant using a reinforcement learning algorithm. The model learned from the data captured by wearable inertial sensors measuring infant leg movement accelerations in an earlier study. Each infant generated a unique model that determined the behavior of the robot. The presented results were obtained from the distributions of the participants' acceleration peaks and demonstrate that the resulting model is sensitive to the degree of differentiation among the participants; each participant (infant) should have his/her own learned policy.This work was supported by NSF award 1706964 (PI: Smith, Co-PI: Matarić). In addition, this work was developed during an international mobility program at the University of Southern California being also partially funded by the European Union ECHORD++ project (FP7-ICT-601116), the LifeBots project (TIN2015-65686-C5) and THERAPIST project (TIN2012-38079)

Dihydropyrimidinase deficiency: structural organization, chromosomal localization, and mutation analysis of the human dihydropyrimidinase gene.

Dihydropyrimidinase (DHP) deficiency (MIM 222748) is characterized by dihydropyrimidinuria and is associated with a variable clinical phenotype. This disease might be associated with a risk of 5-fluorouracil toxicity, although no cases have been reported. We present here both the molecular characterization of the human DHP gene and, for the first time, the mutations causing DHP deficiency. The human DHP gene spans >80 kb and consists of 10 exons. It has been assigned to 8q22, by FISH. We performed mutation analysis of genomic DNA in one symptomatic and five asymptomatic individuals presenting with dihydropyrimidinuria. We identified one frameshift mutation and five missense mutations. Two related Japanese adult subjects were homozygous for the Q334R substitution, whereas two other, unrelated Japanese infant subjects were heterozygous for the same mutation, but this mutation is not common in the Japanese population. A Caucasian pediatric patient exhibiting epileptic attacks, dysmorphic features, and severe developmental delay was homozygous for W360R. Using a eukaryotic expression system, we showed that all mutations reduced enzyme activity significantly, indicating that these are crucial DHP deficiency-causing mutations. There was no significant difference, in residual activity, between mutations observed in the symptomatic and those observed in the asymptomatic individuals