Biology subjects

Roh, K.

Publications and source records attributed to Roh, K..

4 recordsLinked to original sources

bioRxiv2026

Distributed resonant coupling enables high efficiency power transfer to mm-scale bioelectronics

Miniaturized implantable bioelectronics offer breakthrough potential in disease treatment, biomarker monitoring, and physiological sensing. However, wireless power transfer (WPT) remains a central limitation for millimeter-scale devices, as scaling down the receiver size rapidly decreases coupling efficiency due to tissue attenuation, low quality-factors, reduced mutual inductance, and limited tolerance to spatial and angular displacement. Here, we introduce distributed resonant coupling (DRC), a 3-coil WPT paradigm which enables the receiver (Rx) to actively participate in a strongly coupled resonance, transforming the Rx from a passive energy harvester into an active participant in a strongly coupled regime. By co-designing transmitters (Tx), resonators (Rs), and mm-scale receiver coils (Rx) as fully coupled systems, DRC exhibits simulated maximum power levels of 66%, measured received power transfer efficiencies of [~]56%, and end-to-end DC power transfer efficiencies of 42%, delivering >420 mW to loads at 1 W of transmitted power while maintaining robust performance across a range of practically relevant orientations and tissue media. Systematic theoretical and experimental efforts establish core design rules for DRC systems enabling operation without specialized tuning integrated circuits or components. To illustrate the capabilities of DRC in practical applications in vivo, we demonstrate three technologies that capture a broad application space in bioelectronics: implant localization, rapid wireless battery charging, and ultraminiaturized drug delivery devices compatible with particulate drug formulations. Taken together, these results suggest operational capabilities across a wide range of angular tolerances (up to 60{degrees}), tissue depths and dielectric and scattering media.

bioengineering↗

bioRxiv2025

A Novel FNDC1-NAMPT-NAD axis is Implicated in Small and Large-vessel Arterial Disease and Drives Vascular Calcification

Vascular calcification represents a convergent pathological feature of diverse cardiovascular diseases, yet the upstream molecular programs orchestrating this process remain poorly defined. Here, we uncover fibronectin type III domain-containing 1 (FNDC1) as a previously unrecognized regulator of vascular calcification across both microvascular and macrovascular beds. Integrative transcriptomic profiling of human calciphylaxis lesions and atherosclerotic coronaries identified FNDC1 as one of the most significantly upregulated genes. In primary human vascular smooth muscle cells, FNDC1 drove osteogenic phenotype switch and vascular calcification through activation of PI3K/AKT signaling and metabolic reprogramming. Mechanistically, FNDC1 directly binds to nicotinamide phosphoribosyltransferase (NAMPT) resulting in elevated intracellular NAD levels, thus coupling vascular signaling to control of NAD biosynthesis. In murine models, genetic deletion of Fndc1 or pharmacologic inhibition of NAMPT suppressed arterial calcification and prolonged survival. Clinically, circulating FNDC1 levels were elevated in patients with both calciphylaxis and coronary artery disease and independently predicted cardiovascular risk in 42,687 UK Biobank participants. Together, these findings establish FNDC1 as a central mediator of vascular pathology and highlight the FNDC1- NAMPT-NAD+ axis as a promising target for therapeutic intervention.

cell biology↗

bioRxiv2023

Lymphatic muscle cells are unique cells that undergo aging induced changes

Lymphatic muscle cells (LMCs) within the wall of collecting lymphatic vessels exhibit tonic and autonomous phasic contractions, which drive active lymph transport to maintain tissue-fluid homeostasis and support immune surveillance. Damage to LMCs disrupts lymphatic function and is related to various diseases. Despite their importance, knowledge of the transcriptional signatures in LMCs and how they relate to lymphatic function in normal and disease contexts is largely missing. We have generated a comprehensive transcriptional single-cell atlas--including LMCs--of collecting lymphatic vessels in mouse dermis at various ages. We identified genes that distinguish LMCs from other types of muscle cells, characterized the phenotypical and transcriptomic changes in LMCs in aged vessels, and uncovered a pro-inflammatory microenvironment that suppresses the contractile apparatus in advanced-aged LMCs. Our findings provide a valuable resource to accelerate future research for the identification of potential drug targets on LMCs to preserve lymphatic vessel function as well as supporting studies to identify genetic causes of primary lymphedema currently with unknown molecular explanation.

cell biology↗

bioRxiv2017

The evolution of p53 network behavior

We study the evolution of the p53 core regulation network across the taxonomic span of humans to protozoans and nematodes. We introduce a new model for the core regulation network in mammalian cells, and conduct a formal analysis of the different network configurations that emerge in the evolutionary path to complexity. Solving the high dimensional equations associated with this model is typically challenging, and we develop a novel algorithm to overcome this problem. A key technical tool used is the representation of the distinct pathways in the core regulation networks as \"modules\", such that the behavior of the composite of two or more modules can be inferred from the characteristics of each of the individual modules. Apart from simplifying the complexity of the algorithm, this modular representation also allows us to qualitatively compare the distinct types of switching behaviors each network can exhibit. This then allows us to demonstrate how our model for the core regulation network in mammalian cells matches experimentally observed phenomena, and contrast this with the plausible behaviors admitted by the network configurations in putative primordial organisms. We show that the complexity of the p53 core regulation network in vertebrates permits a range of behaviors that can bring about distinct cell fate decisions not possible in the putative primordial organisms.\n\nSignificance StatementThe p53 protein has been protecting organisms from tumors for a billion years. We study the link between the evolution of the p53 network structure and its corresponding tumor suppression strategies. We compare the dynamical behaviors in putative primordial organisms with simple networks with the vertebrate network that contains multiple feedback loops. We show that the vertebrate network, but not the ancestral network, can both repair moderate damage and induce apoptosis if too much damage accumulates, balancing the risk of cancer with the cost of too much cell death. Moreover, the complexity of the vertebrate network allows for adaptation, for example to increase p53 network sensitivity, which is consistent with recent research on large mammals.

systems biology↗