In heart-beat-based security, a security key is derived from the time difference between consecutive heart beats (the inter-pulse interval, IPI), which may, subsequently, be used to enable secure communication. While heart-beat-based security holds promise in mobile health (mHealth) applications, there currently exists no work that provides a detailed characterization of the delivered security in a real system. In this paper, we evaluate the strength of IPI-based security keys in the context of entity authentication. We investigate several aspects that should be considered in practice, including subjects with reduced heart-rate variability (HRV), different sensor-sampling frequencies, intersensor variability (i.e., how accurate each entity may measure heart beats) as well as average and worst-case-authentication time. Contrary to the current state of the art, our evaluation demonstrates that authentication using multiple, less-entropic keys may actually increase the key strength by reducing the effects of intersensor variability. Moreover, we find that the maximal key strength of a 60-bit key varies between 29.2 bits and only 5.7 bits, depending on the subject's HRV. To improve security, we introduce the inter-multi-pulse interval (ImPI), a novel method of extracting entropy from the heart by considering the time difference between nonconsecutive heart beats. Given the same authentication time, using the ImPI for key generation increases key strength by up to 3.4× (+19.2 bits) for subjects with limited HRV, at the cost of an extended key-generation time of 4.8× (+45 s).

Synaptic and intrinsic processing in Purkinje cells, interneurons and granule cells of the cerebellar cortex have been shown to underlie various relatively simple, single-joint, reflex types of motor learning, including eyeblink conditioning and adaptation of the vestibulo-ocular reflex. However, to what extent these processes contribute to more complex, multi-joint motor behaviors, such as locomotion performance and adaptation during obstacle crossing, is not well understood. Here, we investigated these functions using the Erasmus Ladder in cell-specific mouse mutant lines that suffer from impaired Purkinje cell output (Pcd), Purkinje cell potentiation (L7-Pp2b), molecular layer interneuron output (L7-Δγ2), and granule cell output (α6-Cacna1a). We found that locomotion performance was severely impaired with small steps and long step times in Pcd and L7-Pp2b mice, whereas it was mildly altered in L7-Δγ2 and not significantly affected in α6-Cacna1a mice. Locomotion adaptation triggered by pairing obstacle appearances with preceding tones at fixed time intervals was impaired in all four mouse lines, in that they all showed inaccurate and inconsistent adaptive walking patterns. Furthermore, all mutants exhibited altered front–hind and left–right interlimb coordination during both performance and adaptation, and inconsistent walking stepping patterns while crossing obstacles. Instead, motivation and avoidance behavior were not compromised in any of the mutants during the Erasmus Ladder task. Our findings indicate that cell type-specific abnormalities in cerebellar microcircuitry can translate into pronounced impairments in locomotion performance and adaptation as well as interlimb coordination, highlighting the general role of the cerebellar cortex in spatiotemporal control of complex multi-joint movements.