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Mohammad Kohandel

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Published work

7 published item(s)

preprint2026arXiv

Parallel Scan Recurrent Neural Quantum States for Scalable Variational Monte Carlo

Neural-network quantum states have emerged as a powerful variational framework for quantum many-body systems, with recent progress often driven by massively parallel architectures such as transformers. Recurrent neural network quantum states, however, are frequently regarded as intrinsically sequential and therefore less scalable. Here we revisit this view by showing that modern recurrent architectures can support fast, accurate, and computationally accessible neural quantum state simulations. Using autoregressive recurrent wave functions together with recent advances in parallelizable recurrence, we develop variational ansätze, called parallel scan recurrent neural quantum states (PSR-NQS), which can be trained efficiently within variational Monte Carlo in one and two spatial dimensions. We demonstrate accurate benchmark results and show that, with iterative retraining, our approach reaches two-dimensional spin lattices as large as $52\times52$ while remaining in agreement with available quantum Monte Carlo data. Our results establish recurrent architectures as a practical and promising route toward scalable neural quantum state simulations with modest computational resources.

preprint2021arXiv

SARS-CoV-2 quantum sensor based on nitrogen-vacancy centers in diamond

The development of highly sensitive and rapid biosensing tools targeted to the highly contagious virus SARS-CoV-2 is critical to tackling the COVID-19 pandemic. Quantum sensors can play an important role, thanks to their superior sensitivity and fast improvements in recent years. Here we propose a molecular transducer designed for nitrogen-vacancy (NV) centers in nanodiamonds, translating the presence of SARS-CoV-2 RNA into an unambiguous magnetic noise signal that can be optically read out. We evaluate the performance of the hybrid sensor, including its sensitivity and false negative rate, and compare it to widespread diagnostic methods. The proposed method is fast and promises to reach a sensitivity down to a few hundreds of RNA copies with false negative rate less than 1%. The proposed hybrid sensor can be further implemented with different solid-state defects and substrates, generalized to diagnose other RNA viruses, and integrated with CRISPR technology.

preprint2015arXiv

Modelling Invasion Dynamics with Spatial Random-Fitness due to Microenvironment

Numerous experimental studies have demonstrated that the microenvironment is a key regulator influencing the proliferative and migrative potentials of species. Spatial and temporal disturbances lead to adverse and hazardous microenvironments for cellular systems that is reflected in the phenotypic heterogeneity within the system. In this paper, we study the effect of microenvironment on the invasive capability of species, or mutants, on structured grids under the influence of site-dependent random proliferation in addition to a migration potential. We discuss both continuous and discrete fitness distributions. Our results suggest that the invasion probability is negatively correlated with the variance of fitness distribution of mutants (for both advantageous and neutral mutants) in the absence of migration of both types of cells. A similar behaviour is observed even in the presence of a random fitness distribution of host cells in the system with neutral fitness rate. In the case of a bimodal distribution, we observe zero invasion probability until the system reaches a (specific) proportion of advantageous phenotypes. Also, we find that the migrative potential amplifies the invasion probability as the variance of fitness of mutants increases in the system, which is the exact opposite in the absence of migration. Our computational framework captures the harsh microenvironmental conditions through quenched random fitness distributions and migration of cells, and our analysis shows that they play an important role in the invasion dynamics of several biological systems such as bacterial micro-habitats, epithelial dysplasia, and metastasis. We believe that our results may lead to more experimental studies, which can in turn provide further insights into the role and impact of heterogeneous environments on invasion dynamics.

preprint2014arXiv

Modeling Age-Dependent Radiation-Induced Second Cancer Risks and Estimation of Mutation Rate: An Evolutionary Approach

Although the survival rate of cancer patients has significantly increased due to advances in anti-cancer therapeutics, one of the major side effects of these therapies, particularly radiotherapy, is the potential manifestation of radiation-induced secondary malignancies. In this work, a novel evolutionary stochastic model is introduced that couples short-term formalism (during radiotherapy) and long-term formalism (post treatment). This framework is used to estimate the risks of second cancer as a function of spontaneous background and radiation-induced mutation rates of normal and pre-malignant cells. By fitting the model to available clinical data for spontaneous background risk together with data of Hodgkins lymphoma survivors (for various organs), the second cancer mutation rate is estimated. The model predicts a significant increase in mutation rate for some cancer types, which may be a sign of genomic instability. Finally, it is shown that the model results are in agreement with the measured results for excess relative risk (ERR) as a function of exposure age, and that the model predicts a negative correlation of ERR with increase in attained age. This novel approach can be used to analyze several radiotherapy protocols in current clinical practice, and to forecast the second cancer risks over time for individual patients.

preprint2014arXiv

Replicator Dynamics of of Cancer Stem Cell; Selection in the Presence of Differentiation and Plasticity

Stem cells have the potential to produce lineages of non-stem cell populations (differentiated cells) via a ubiquitous hierarchal division scheme. Differentiation of a stem cell into (partially) differentiated cells can happen either symmetrically or asymmetrically. The selection dynamics of a mutant cancer stem cell should be investigated in the light of a stem cell proliferation hierarchy and presence of a non-stem cell population. By constructing a three-compartment Moran-type model composed of normal stem cells, mutant (cancer) stem cells and differentiated cells, we derive the replicator dynamics of stem cell frequencies where asymmetric differentiation and differentiated cell death rates are included in the model. We determine how these new factors change the conditions for a successful mutant invasion and discuss the variation on the steady state fraction of the population as different model parameters are changed. By including the phenotypic plasticity/dedifferentiation, in which a progenitor/differentiated cell can transform back into a cancer stem cell, we show that the effective fitness of mutant stem cells is not only determined by their proliferation and death rates but also according to their dedifferentiation potential. By numerically solving the model we derive the phase diagram of the advantageous and disadvantageous phases of cancer stem cells in the space of proliferation and dedifferentiation potentials. The result shows that at high enough dedifferentiation rates even a previously disadvantageous mutant can take over the population of normal stem cells. This observation has implications in different areas of cancer research including experimental observations that imply metastatic cancer stem cell types might have lower proliferation potential than other stem cell phenotypes while showing much more phenotypic plasticity and can undergo clonal expansion.

preprint2014arXiv

The duality of spatial death-birth and birth-death processes and limitations of the isothermal theorem

Evolutionary models on graphs, as an extension of the Moran process, have two major implementations: birth-death (BD) models (or the invasion process) and death- birth (DB) models (or voter models). The isothermal theorem states that the fixation probability of mutants in a large group of graph structures (known as isothermal graphs, which include regular graphs) coincides with that for the mixed population. This result has been proven by Lieberman et al (Nature 433: 312-316, 2005) in the case of BD processes, where mutants differ from the wild types by their birth rate (and not by their death rate). In this paper we discuss to what extent the isothermal theorem can be formulated for DB processes, proving that it only holds for mutants that differ from the wild type by their death rate (and not by their birth rate). For more general BD and DB processes with arbitrary birth and death rates of mutants, we show that the fixation probabilities of mutants are different from those obtained in the mass-action populations. We focus on spatial lattices and show that the difference between BD and DB processes on 1D and 2D lattices are non-small even for large population sizes. We support these results with a generating function approach that can be generalized to arbitrary graph structures. Finally, we discuss several biological applications of the results.

preprint2013arXiv

Stochastic Model for Tumor Control Probability: Effects of Cell Cycle and (A)symmetric Proliferation

Estimating the required dose in radiotherapy is of crucial importance since the administrated dose should be sufficient to eradicate the tumor and at the same time should inflict minimal damage on normal cells. The probability that a given dose and schedule of ionizing radiation eradicates all the tumor cells in a given tissue is called the tumor control probability (TCP), and is often used to compare various treatment strategies used in radiation therapy. In this paper, we aim to investigate the effects of including cell-cycle phase on the TCP by analyzing a stochastic model of a tumor comprised of actively dividing cells and quiescent cells with different radiation sensitivities. We derive an exact phase-diagram for the steady-state TCP of the model and show that at high, clinically-relevant doses of radiation, the distinction between active and quiescent tumor cells (i.e. accounting for cell-cycle effects) becomes of negligible importance in terms of its effect on the TCP curve. However, for very low doses of radiation, these proportions become significant determinants of the TCP. Moreover, we use a novel numerical approach based on the method of characteristics for partial differential equations, validated by the Gillespie algorithm, to compute the TCP as a function of time. We observe that our results differ from the results in the literature using similar existing models, even though similar parameters values are used, and the reasons for this are discussed.