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Azadi, A.

Publications and source records attributed to Azadi, A..

2 recordsLinked to original sources

Handwritten Digit classification with neural cultures is influenced by neural architecture, network dynamics, and decoding methods

As silicon-based computing approaches fundamental physical limits, neurocomputing offers an energy-efficient alternative by leveraging the intrinsic non-linear dynamics of biological systems. To harness these dynamics, it is vital to understand the structure-function relationship governing how neural cultures process complex spatio-temporal information and how to appropriately decode the resulting neural electrophysiological activity. We investigated this utilizing a closed-loop electrophysiology platform, the CL1, to implement reservoir computing in human iPSC-derived neuronal networks. To systematically evaluate the variables driving neurocomputational capacity, we explored how cellular composition (cortical vs. hippocampal lineages), and the physical architecture (unstructured monolayers, 3D neural organoids, and modular networks confined by microfluidic devices) influenced electrophysiological properties and interacted with different decoding methodologies. Using a spatio-temporal version of a handwritten digit pattern recognition task (MNIST), we analyzed how these biological and analytical factors influenced classification accuracy. To ensure robust interpretation this required us to first demonstrated that reservoir computing decoding methods require strict artifact control and trial-based cross-validation to distinguish network computation from artifactual signal separability or temporal data leakage. Applying this validated frequency-domain pipeline, we suggest a clear functional hierarchy where structural modularity acts as a vital functional regularizer. Modular cortical cultures significantly outperformed unconstrained monolayers and organoids on MNIST. Furthermore, decoding frequency information from raw signals proved superior to typical time-bin decoding implementations. These findings establish that maximizing the computational potential of Synthetic Biological Intelligence, while avoiding false positives, requires a synergistic optimization of cellular identity, structural governance, and rigorous decoding logic. In doing so, this work provides a critical base establishing the criteria under which to evaluate neurocomputing implementations.

neuroscience↗

Dynamic Modeling of Signal Transduction by mTOR Complexes in Cancer

Signal integration in the mTOR pathway plays a vital role in cell fate decision making in cancer cells. As a signal integrator, mTOR shows a complex dynamical behavior which determines the cell fate at different cellular processes levels including cell cycle progression, cell survival, cell death, metabolic reprogramming, and aging. The dynamics of the complex responses to rapamycin in cancer cells have been attributed to its differential time-dependent inhibitory effects on mTORC1 and mTORC2, the two main complexes of mTOR. Two explanations were previously provided for this phenomenon: 1-Rapamycin does not inhibit mTORC2 directly, whereas it prevents mTORC2 formation by sequestering free mTOR protein. 2-Components like Phosphatidic Acid further stabilize mTORC2 compared with mTORC1. To understand the mechanism by which rapamycin differentially inhibits the mTOR complexes, we present a mathematical model of rapamycin mode of action based on the first explanation, i.e., Le Chateliers principle. Translating the interactions among components of mTORC1 and mTORC2 into a mathematical model revealed the dynamics of rapamycin action in different doses and time-intervals of rapamycin treatment. The model shows that rapamycin has stronger effects on mTORC1 compared with mTORC2, simply due to its direct interaction with free mTOR and mTORC1, but not mTORC2, without the need to consider other components that might further stabilize mTORC2. Based on our results, even when mTORC2 is less stable compared with mTORC1, it can be less inhibited by rapamycin.

systems biology↗