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Namshik Han

Publications and source records attributed to Namshik Han.

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Universal scaling and protocol-dependent amplitude in hybrid quantum walks

Quantum walks spread ballistically but become diffusive with classical admixture. We compare two hybrid walks using identical quantum and classical steps at the same classical-step rate but ordered differently in time. Any nonzero admixture yields diffusion. Near the quantum limit, both diffusion coefficients have first-order poles, but their amplitudes differ by about a factor of two. The coherence timescale sets the pole order, while temporal organization sets the amplitude. We expect our analytical framework to apply broadly to quantum--classical hybrid systems.

quant-ph

Advancing Understanding of Long COVID Pathophysiology Through Quantum Walk-Based Network Analysis

Long COVID is a multisystem condition characterized by persistent symptoms such as fatigue, cognitive impairment, and systemic inflammation, following COVID-19 infection, yet its mechanisms remain poorly understood. In this study, we applied quantum walk (QW), a computational approach leveraging quantum interference, to explore large-scale SARS-CoV-2-induced protein (SIP) networks. Compared to the conventional random walk with restart (RWR) method, QW demonstrated superior capacity to traverse deeper regions of the network, uncovering proteins and pathways implicated in Long COVID. Key findings include mitochondrial dysfunction, thromboinflammatory responses, and neuronal inflammation as central mechanisms. QW uniquely identified the CDGSH iron-sulfur domain-containing protein family and VDAC1, a mitochondrial calcium transporter, as critical regulators of these processes. VDAC1 emerged as a potential biomarker and therapeutic target, supported by FDA-approved compounds such as cannabidiol. These findings highlight QW as a powerful tool for elucidating complex biological systems and identifying novel therapeutic targets for conditions like Long COVID.

q-bio.MN

An in silico drug repurposing pipeline to identify drugs with the potential to inhibit SARS-CoV-2 replication

Drug repurposing provides an opportunity to redeploy drugs, which ideally are already approved for use in humans, for the treatment of other diseases. For example, the repurposing of dexamethasone and baricitinib has played a crucial role in saving patient lives during the ongoing SARS-CoV-2 pandemic. There remains a need to expand therapeutic approaches to prevent life-threatening complications in patients with COVID-19. Using an in silico approach based on structural similarity to drugs already in clinical trials for COVID-19, potential drugs were predicted for repurposing. For a subset of identified drugs with different targets to their corresponding COVID-19 clinical trial drug, a mechanism of action analysis was applied to establish whether they might have a role in inhibiting the replication of SARS-CoV-2. Of sixty drugs predicted in this study, two with the potential to inhibit SARS-CoV-2 replication were identified using mechanism of action analysis. Triamcinolone is a corticosteroid that is structurally similar to dexamethasone; gallopamil is a calcium channel blocker that is structurally similar to verapamil. In silico approaches indicate possible mechanisms of action for both drugs in inhibiting SARS-CoV-2 replication. The identification of these drugs as potentially useful for patients with COVID-19 who are at a higher risk of developing severe disease supports the use of in silico approaches to facilitate quick and cost-effective drug repurposing. Such drugs could expand the number of treatments available to patients who are not protected by vaccination.

q-bio.QM