Publications by authors named "I A Soloviev"

In this article, we consider designs of simple analog artificial neural networks based on adiabatic Josephson cells with a sigmoid activation function. A new approach based on the gradient descent method is developed to adjust the circuit parameters, allowing efficient signal transmission between the network layers. The proposed solution is demonstrated on the example of a system that implements XOR and OR logical operations.

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We have studied the proximity effect in an SF1S1F2s superconducting spin valve consisting of a massive superconducting electrode (S) and a multilayer structure formed by thin ferromagnetic (F1,2) and superconducting (S1, s) layers. Within the framework of the Usadel equations, we have shown that changing the mutual orientation of the magnetization vectors of the F1,2 layers from parallel to antiparallel serves to trigger superconductivity in the outer thin s-film. We studied the changes in the pair potential in the outer s-film and found the regions of parameters with a significant spin-valve effect.

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Josephson digital or analog ancillary circuits are an essential part of a large number of modern quantum processors. The natural candidate for the basis of tuning, coupling, and neromorphic co-processing elements for processors based on flux qubits is the adiabatic (reversible) superconducting logic cell. Using the simplest implementation of such a cell as an example, we have investigated the conditions under which it can optionally operate as an auxiliary qubit while maintaining its "classical" neural functionality.

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The imitative modelling of processes in the brain of living beings is an ambitious task. However, advances in the complexity of existing hardware brain models are limited by their low speed and high energy consumption. A superconducting circuit with Josephson junctions closely mimics the neuronal membrane with channels involved in the operation of the sodium-potassium pump.

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We studied the state of the DNA repair system and apoptosis in young mice carrying heterozygous inactivating mutation in the NBS1 gene (c.1971insT, p.Arg658Stop).

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