Towards an emotion-driven interactive music system: ridging the gaps between affect, physiology and sound generation

Report for the scientific sojourn at the Stanford University from January until June 2007. Music is well known for affecting human emotional states, yet the relationship between specific musical parameters and emotional responses is still not clear. With the advent of new human-computer interaction (HCI) technologies, it is now possible to derive emotion-related information from physiological data and use it as an input to interactive music systems. Providing such implicit musical HCI will be highly relevant for a number of applications including music therapy, diagnosis, nteractive gaming, and physiologically-based musical instruments. A key question in such physiology-based compositions is how sound synthesis parameters can be mapped to emotional states of valence and arousal. We used both verbal and heart rate responses to evaluate the affective power of five musical parameters. Our results show that a significant correlation exists between heart rate and the subjective evaluation of well-defined musical parameters. Brightness and loudness showed to be arousing parameters on subjective scale while harmonicity and even partial attenuation factor resulted in heart rate changes typically associated to valence. This demonstrates that a rational approach to designing emotion-driven music systems for our public installations and music therapy applications is possible.

Sex Reversal in Zebrafish fancl Mutants is Caused by Tp53-Mediated Germ Cell Apoptosis

The molecular genetic mechanisms of sex determination are not known for most vertebrates, including zebrafish. We identified a mutation in the zebrafish fancl gene that causes homozygous mutants to develop as fertile males due to female-to-male sex reversal. Fancl is a member of the Fanconi Anemia/BRCA DNA repair pathway. Experiments showed that zebrafish fancl was expressed in developing germ cells in bipotential gonads at the critical time of sexual fate determination. Caspase-3 immunoassays revealed increased germ cell apoptosis in fancl mutants that compromised oocyte survival. In the absence of oocytes surviving through meiosis, somatic cells of mutant gonads did not maintain expression of the ovary gene cyp19a1a and did not down-regulate expression of the early testis gene amh; consequently, gonads masculinized and became testes. Remarkably, results showed that the introduction of a tp53 (p53) mutation into fancl mutants rescued the sex-reversal phenotype by reducing germ cell apoptosis and, thus, allowed fancl mutants to become fertile females. Our results show that Fancl function is not essential for spermatogonia and oogonia to become sperm or mature oocytes, but instead suggest that Fancl function is involved in the survival of developing oocytes through meiosis. This work reveals that Tp53-mediated germ cell apoptosis induces sex reversal after the mutation of a DNA-repair pathway gene by compromising the survival of oocytes and suggests the existence of an oocyte-derived signal that biases gonad fate towards the female developmental pathway and thereby controls zebrafish sex determination.