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In the traditional public key cryptosystem based on certificates, the issuance and management of user certificates are realized through the authoritative certificate center, but amount of time is spent in the transmission and verification of user public key certificates. After a malicious user obtaining legitimate users' private keys, he can select a secret value and signature process to generate the final private key, public key and signature. And he will announce that he is the legal user, while others are unable to distinguish this process. This is the defect of traditional digital signature scheme without certificate. Therefore, this paper proposes a certificateless short signature scheme based on integrated neural networks and elliptic curve cryptography for secure data fusion analysis. The security of the solution is based on Inv-CDH problem. The complete security proof is given under the stochastic predictor model. It is proved that the new model can resist existence forgery in adaptive selective message attack with new adversary. Experiment results show that the calculation amount of our proposed certificateless short signature scheme is small and the efficiency is high compared with other state-of-the-art schemes. [ABSTRACT FROM AUTHOR]

Breathing in mammals depends on rhythms that originate from the preBötzinger complex (preBötC) of the ventral medulla and a network of brainstem and spinal premotor neurons. The rhythm-generating core of the preBötC, as well as some premotor circuits, consist of interneurons derived from Dbxl-expressing precursors (Dbxl neurons), but the structure and function of these networks remain incompletely understood. We previously developed a cell-specific detection and laser ablation system to interrogate respiratory network structure and function in a slice model of breathing that retains the preBötC, the respiratory-related hypoglossal (XII) motor nucleus and XII premotor circuits. In spontaneously rhythmic slices, cumulative ablation of Dbxl preBötC neurons decreased XII motor output by -50% after -15 cell deletions, and then decelerated and terminated rhythmic function altogether as the tally increased to -85 neurons. In contrast, cumulatively deleting Dbxl XII premotor neurons decreased motor output monotonically but did not affect frequency nor stop XII output regardless of the ablation tally. Here, we couple an existing preBötC model with a premotor population in several topological configurations to investigate which one may replicate the laser ablation experiments best. If the XII premotor population is a "small-world" network (rich in local connections with sparse long-range connections among constituent premotor neurons) and connected with the preBötC such that the total number of incoming synapses remains fixed, then the in silico system successfully replicates the in vitro laser ablation experiments. This study proposes a feasible configuration for circuits consisting of Dbxl-derived interneurons that generate inspiratory rhythm and motor pattern. [ABSTRACT FROM AUTHOR]

How brain functions degenerate in the face of progressive cell loss is an important issue that pertains to neurodegenerative diseases and basic properties of neural networks. We developed an automated system that uses two-photon microscopy to detect rhythmic neurons from calcium activity, and then individually laser ablates the targets while monitoring network function in real time. We applied this system to the mammalian respiratory oscillator located in the pre-Bötzinger Complex (preBötC) of the ventral medulla, which spontaneously generates breathing-related motor activity in vitro. Here, we show that cumulatively deleting preBötC neurons progressively decreases respiratory frequency and the amplitude of motor output. On average, the deletion of 120 ± 45 neurons stopped spontaneous respiratory rhythm, and our data suggest ≈82% of the rhythm-generating neurons remain unlesioned. Cumulative ablations in other medullary respiratory regions did not affect frequency but diminished the amplitude of motor output to a lesser degree. These results suggest that the preBötC can sustain insults that destroy no more than ≈18% of its constituent interneurons, which may have implications for the onset of respiratory pathologies in disease states. [ABSTRACT FROM AUTHOR]