Modeling speech imitation and ecological learning of auditory-motor maps.

Classical models of speech consider an antero-posterior distinction between perceptive and productive functions. However, the selective alteration of neural activity in speech motor centers, via transcranial magnetic stimulation, was shown to affect speech discrimination. On the automatic speech recognition (ASR) side, the recognition systems have classically relied solely on acoustic data, achieving rather good performance in optimal listening conditions. The main limitations of current ASR are mainly evident in the realistic use of such systems. These limitations can be partly reduced by using normalization strategies that minimize inter-speaker variability by either explicitly removing speakers' peculiarities or adapting different speakers to a reference model. In this paper we aim at modeling a motor-based imitation learning mechanism in ASR. We tested the utility of a speaker normalization strategy that uses motor representations of speech and compare it with strategies that ignore the motor domain. Specifically, we first trained a regressor through state-of-the-art machine learning techniques to build an auditory-motor mapping, in a sense mimicking a human learner that tries to reproduce utterances produced by other speakers. This auditory-motor mapping maps the speech acoustics of a speaker into the motor plans of a reference speaker. Since, during recognition, only speech acoustics are available, the mapping is necessary to "recover" motor information. Subsequently, in a phone classification task, we tested the system on either one of the speakers that was used during training or a new one. Results show that in both cases the motor-based speaker normalization strategy slightly but significantly outperforms all other strategies where only acoustics is taken into account

Modulation of aflatoxin B1 cytotoxicity and aflatoxin M1 synthesis by natural antioxidants in a bovine mammary epithelial cell line

Aflatoxin (AF) B1, a widespread food and feed contaminant, is bioactivated by drug metabolizing enzymes (DME) to cytotoxic and carcinogenic metabolites like AFB1-epoxide and AFM1, a dairy milk contaminant. A number of natural antioxidants have been reported to afford a certain degree of protection against AFB1 (cyto)toxicity. As the mammary gland potentially participates in the generation of AFB1 metabolites, we evaluated the role of selected natural antioxidants (i.e. curcumin, quercetin and resveratrol) in the modulation of AFB1 toxicity and metabolism using a bovine mammary epithelial cell line (BME-UV1). Quercetin and, to a lesser extent, resveratrol and curcumin from Curcuma longa (all at 5 \u3bcM) significantly counteracted the AFB1-mediated impairment of cell viability (concentration range: 96\u2013750 nM). Moreover, quercetin was able to significantly reduce the synthesis of AFM1. The quantitative PCR analysis on genes encoding for DME (phase I and II) and antioxidant enzymes showed that AFB1 caused an overall downregulation of the detoxifying systems, and mainly of GSTA1, which mediates the GSH conjugation of the AFB1-epoxide. The negative modulation of GSTA1 was efficiently reversed in the presence of quercetin, which significantly increased GSH levels as well. It is suggested that quercetin exerts its beneficial effects by depressing the bio-transformation of AFB1 and counterbalancing its pro-oxidant effects