Biology subjects

Chatterjee, B.

Publications and source records attributed to Chatterjee, B..

At least 19 recordsLinked to original sources

bioRxiv2026

2-arm-PEG-oligocations transiently shield the liver sinusoids to mitigate off-target hepatic expression of mRNA lipid nanoparticles

Ionizable lipid nanoparticles (iLNPs) are powerful platforms for mRNA-based vaccines and immunotherapies; however, their intrinsic liver tropism compromises both safety and efficacy. Off-target hepatic protein expression from delivered mRNA raises safety concerns, and hepatic clearance limits efficient iLNP delivery to target organs. In this study, we address these challenges in mouse models by stealth-coating the liver sinusoidal endothelial (LSE) wall, the primary gateway for nanoparticle entry into the liver. Specifically, oligocations conjugated with two-armed PEG (2-arm-PEG-oligocations), a clinically relevant material used in oligonucleotide delivery trials, were employed to transiently anchor PEG to the LSE wall with balanced affinity, ensuring robust coating followed by gradual biliary clearance. This approach reduced hepatic protein expression from iLNPs, subsequently administered either systemically or locally, by more than tenfold. Importantly, the strategy preserved iLNP accumulation in the spleen, a key target organ for vaccines, effectively redirecting iLNPs from the liver to the spleen. Consequently, in vaccine applications, pre-injection of the 2-arm-PEG-oligocation preserved or even enhanced vaccination efficacy while minimizing concerns associated with antigen expression in the liver. In applications involving cytokine mRNA therapy, specifically intratumoral interleukin-12 (IL-12) mRNA administration, systemic pre-injection of the 2-arm-PEG-oligocation successfully reduced off-target hepatic IL-12 expression and subsequent systemic IL-12 exposure, while maintaining antitumor efficacy. Collectively, these results demonstrate that LSE-wall stealth coating is a generalizable strategy to improve both the safety and efficacy of iLNP-based mRNA vaccines and immunotherapies.

bioengineering↗

bioRxiv2026

The active secretion of a subunit of IL-12 by tissue cells is regulated by Valosin-Containing Protein and intracellular calcium redistribution.

One molecular mechanism for collaboration between innate immune and tissue stromal cells in regulating effector responses is the formation of the innate cytokine IL-12 as a result of the two cell types contributing distinct subunits (p40 and p35) allowing for the localized assembly of the functional IL-12 heterodimer. Dendritic cell activation leads to p40 secretion, but the pathways in stromal cells allowing p35 secretion are unknown. We identify the inhibition of Valosin-Containing Protein (VCP) and increases in intracellular calcium signaling as the key regulators for the secretion of p35 from its homeostatic reservoirs in the endoplasmic reticulum. This p35 secretion, in the absence of co-expression of the p40 subunit, requires active gene expression, is independent of ER stress pathways, and is distinct from passive (cell-death dependent) release processes. Thus, an active sensory apparatus in non-hematopoietic cells contributes to the collaborative control of the trajectory of early immune differentiation. One Sentence SummaryVCP inhibition and calcium flux allows stromal cells to release the p35 subunit of the cytokine IL-12 and regulate localized cytokine activity.

immunology↗

bioRxiv2025

Role of Myc family proteins in transcriptional regulation of growth and oncogenic transformation in fusion-positive rhabdomyosarcoma

Fusion-positive rhabdomyosarcoma (FP-RMS) is driven by a PAX3::FOXO1 (P3F) or PAX7::FOXO1 fusion gene. After finding that MYCN is required for P3F-induced oncogenic transformation in a human myoblast model of FP-RMS, we further investigated the role of Myc family proteins in FP-RMS. Expression studies revealed that myoblast models and a subset of FP-RMS lines have predominant MYCN or MYC expression whereas other FP-RMS lines have both high MYCN and MYC expression. In myoblast models, MYCN was required for optimal P3F binding to and high-level activation of FGF8, a P3F target that is necessary and sufficient for oncogenic transformation. MYCN or MYC knockdown suppressed transformation in myoblast and FP-RMS lines with dominant MYCN or MYC expression, respectively. In FP-RMS lines with high MYCN and MYC expression, there was partial loss of transformation when one gene was targeted and complete loss when both genes were targeted. Despite the loss of oncogenic activity in lines with knockdown of a dominant Myc family member, FGF8 expression was not decreased. Transcriptomic analyses revealed that P3F target genes were not affected by MYCN or MYC knockdown, and instead a group of Myc-specific targets was down-regulated. Collectively, these results indicate that MYCN or MYC is functionally dominant in myoblast models and FP-RMS lines with dominant expression of one Myc family protein whereas MYCN and MYC are functionally redundant in FP-RMS cell lines with high expression of both. These Myc family proteins contribute to oncogenic properties by facilitating P3F activation of FGF8 and increasing expression of Myc-specific targets.

cancer biology↗

bioRxiv2025

ATRX Loss Predicts Poor Outcomes and Reveals a Therapeutic Vulnerability to TEAD Inhibition in Soft Tissue Sarcomas

ATRX is one of the most frequently altered genes in sarcoma and encodes an ATP-dependent chromatin remodeler implicated in maintaining heterochromatin. However, ATRX alterations have not been leveraged for sarcoma treatment. We observed loss of ATRX protein in 14% of soft tissue leiomyosarcoma (STLMS, n =127), 53% of uterine leiomyosarcoma (ULMS, n = 95), 37% of undifferentiated pleomorphic sarcoma (UPS, n = 82), and 8% of dedifferentiated liposarcoma (DDLPS, n = 84). ATRX loss was associated with significantly worse outcomes in ULMS, UPS, and DDLPS. ATRX knockout in sarcoma cells increased proliferation in cooperation with TP53 deletion. ATRX knockout led to chromatin de-repression and enrichment of PRDM4 and NFIX transcription factor (TF) motifs. PRDM4 and NFIX knockdown in ATRX-mutant sarcoma lines resulted in reduced proliferation and invasion suggesting epistatic relationship. Consistent with the known functional relationship between PRMD4 and YAP1, we observed that ATRX/TP53 KO cells were more sensitive to the TEAD inhibitor VT103 compared to TP53 KO and ATRX WT controls. Overall, our results identify ATRX loss as a prognostic factor of worse outcomes, implicate the ATRX-PRDM4-YAP1 axis as a novel underlying mechanism, and suggest use of TEAD inhibition as a potential therapeutic strategy for ATRX-deficient sarcomas. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=45 SRC="FIGDIR/small/689992v1_ufig1.gif" ALT="Figure 1"> View larger version (13K): org.highwire.dtl.DTLVardef@a759ecorg.highwire.dtl.DTLVardef@100c580org.highwire.dtl.DTLVardef@1a675c9org.highwire.dtl.DTLVardef@17f1f91_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

bioRxiv2025

Proteus mirabilis entails a switch from commensal to pathogen - Genomic insights from a blaTEM-1B-harboring novel isolate from India.

BackgroundProteus mirabilis is an opportunistic pathogen that can shift from gut commensalism to causing severe urinary tract and bloodstream infections. The genomic basis of P. mirabilis transition from commensalism to severe infection is not well understood, especially in Indian clinical isolates. This study aimed to explore the genomic attributes of a prevalent P. mirabilis strain in India. MethodsWhole-genome sequencing (WGS) was performed on a clinical P. mirabilis isolate by using NGS. AMR genes and virulence factors were identified using ResFinder/CARD and VFDB, respectively. Sequence typing was performed with MLST. Protein-protein interactions and noncoding RNAs were analyzed using STRING, CytoHubba, and BAKTA. ResultsWGS confirmed the multidrug-resistant nature of the isolate, revealing a broad repertoire of AMR genes, including blaTEM-1B, conferring resistance to beta-lactam antibiotics. Several resistance determinants were co-localised with insertion sequences on a single contig, indicating a high potential for horizontal gene transfer. The virulome profile highlighted multiple fimbrial genes, hemolysins, and toxin-encoding loci, together supporting strong adhesion, biofilm formation, and host tissue damage. Comparative analysis revealed unique genomic signatures not present in reference isolates, including additional virulence determinants and mobile genetic elements. MLST profile of the isolate is closely related to ST-675 & ST-797, while virulence typing (vST-1157) indicated a novel profile distinct from reference ST-675 strains. Insilico protein-protein interaction of this isolate revealed a highly interconnected virulence network, with urease, fimbrial adhesins, and hemolysins emerging as central functional modules driving pathogenicity. In addition, a noncoding RNA was identified within the genomic context of the ure operon (Contig 10), suggesting a possible regulatory role in urease expression. PPI network analysis highlighted urease, fimbrial proteins, and hemolysins as central hubs contributing to pathogenicity. ConclusionsThis study presents the first genomic characterization of a multidrug-resistant P. mirabilis clinical isolate from India, designated as P. mirabilis strain Indica. The convergence of AMR genes, virulence factors, MGEs and a novel noncoding RNAs linked to urease expression highlights the emergence of a high-risk variant in India. These findings have significant implications for infection control and emphasize the need for genomic surveillance to guide therapeutic strategies and develop new interventions globally.

microbiology↗

bioRxiv2025

Differential Tissue Coupled Powering for Battery-Free Injectable Electroceuticals

Electroceutical implants that deliver targeted neural stimulation have shown therapeutic potential for a wide range of neurological and peripheral disorders, yet wirelessly powering ultra-miniaturized, fully injectable systems remains a critical challenge. Here we report a Thread-like Injectable Neural TechnologY (TINY), powered via a differential tissue-coupled powering (DTCP) scheme. DTCP employs mid-frequency differential potentials applied across external electrodes on a compact, wearable transmitter to deliver energy through tissue to an ultra-miniaturized, thread-like implant that integrates a custom ASIC and PEDOT-coated receiver and stimulation electrodes. Benchtop experiments in agar phantoms characterize the power-transfer efficiency (PTE) and reveal that PTE increases with implant length while maintaining strong tolerance to angular misalignment. In vivo tests in rat hindlimbs further demonstrate wireless activation of the sciatic nerve through tissue at centimeter-scale depths, confirming effective transcutaneous energy delivery for neurostimulation. A 20-day implantation study shows stable positioning of the device with minimal tissue response, indicating excellent chronic compatibility. These findings address long-standing challenges in wirelessly powering injectable electroceuticals and establish DTCP as a scalable and alignment-robust powering strategy for future minimally invasive neuromodulation therapies.

bioengineering↗

bioRxiv2025

Moderated designs can balance between batch-effect mitigation and cell loss due to hashtag-assisted pooling in single-cell experiments

Minimizing experimental noise is integral to robust data generation in single-cell science. Experimental processing of different samples as a single pool, made possible by hashtag-assisted pooling, helps minimize batch-effects, but the computational demultiplexing of the data can also lead to loss of cells whose hashtags cannot be resolved accurately. Here, we examine four alternate experimental designs that could be used instead of a single-pool approach and quantify the batch effects as well as cell loss in each case. While a reference design offers the best performance, this study can help individual investigators choose one suited for their biological questions.

bioinformatics↗

bioRxiv2025

Fusion transcription factor dosage controls cell state in rhabdomyosarcoma

In the fusion-positive subset of rhabdomyosarcoma, the PAX3::FOXO1 oncoprotein is the most common fusion driver. We previously established a human myoblast system for inducible expression of PAX3::FOXO1. In the current study, we modulate PAX3::FOXO1 protein expression to understand the epigenetic and phenotypic functions at different PAX3::FOXO1 levels. Proliferative and oncogenic outcomes depend on PAX3::FOXO1 dosage in this system with transformation dominant at intermediate levels and growth suppression dominant at high levels. After prolonged PAX3::FOXO1 expression, there is dosage-dependent heterogeneity in single cell gene expression profiles. We observe a dosage-specific effect for PAX3::FOXO1 chromatin recognition and identify factors that modulate PAX3::FOXO1 chromatin binding. PAX3::FOXO1 dosage affects expression signatures related to cell cycle, epithelial-mesenchymal transition, and myogenesis. Whereas intermediate PAX3::FOXO1 expression maximizes chromatin binding to modulate gene expression, high PAX3::FOXO1 expression alters S phase progression and increases accessibility behind the replication fork. We conclude that PAX3::FOXO1 exerts dosage-dependent functions to influence epigenetic heterogeneity in fusion-positive rhabdomyosarcoma.

genomics↗

bioRxiv2025

Endothelial Cu Uptake Transporter CTR1 Senses Disturbed Flow to Promote Atherosclerosis through Cuproptosis

Endothelial cells (ECs) lining blood vessels sense disturbed blood flow (D-flow), which drives mitochondrial dysfunction and atherosclerosis. Copper (Cu) is an essential micronutrient, and its disruption of homeostasis has been implicated in atherosclerosis. Cellular Cu levels are tightly controlled by Cu transport proteins including the Cu importer CTR1. Cuproptosis is a recently discovered form of regulated cell death triggered by mitochondrial Cu accumulation, but its endogenous stimulants and role in atherosclerosis remain unknown. Using EC-specific CTR1-deficient mice and cultured ECs, we show that endothelial CTR1 responds to D-flow by increasing mitochondrial Cu levels through its interaction with the mitochondrial Cu transporter SLC25A3 at caveolae/lipid rafts. This leads to the aggregation of lipoylated mitochondrial proteins, mitochondrial dysfunction, and cuproptosis, thereby exacerbating atherosclerosis. Importantly, mitochondria-targeted Cu-chelating nanoparticles effectively mitigate D-flow-induced cuproptosis and atherosclerosis, highlighting the endothelial CTR1-SLC25A3-mitochondrial Cu axis as a potential therapeutic target.

cell biology↗

bioRxiv2024

Kinetic patterns of single cell gene expression discriminate between the murine cellular responses to live attenuated and inactivated Yellow Fever vaccines

The success of the live attenuated Yellow Fever vaccine (YF17D) that elicits immunity lasting over thirty years has made it a widely used model to understand the generation of durable protection. We compare the early single-cell level transcriptional response in mice to YF17D and an adjuvanted-inactivated, but less effective version (InYF). Within the first week, we identify 70 kinetic patterns in 45 cellular clusters, majority of which discriminate between the two formulations, some in a tissue and sex-specific manner. Intriguingly, differential transcripts fall into two categories, one whose association with YF17D or InYF is maintained even when decoupled from their cell-type of expression and the other where such cell-plus-gene pairing is critical to maintain differential marker status. We demonstrate applications of this resource, by identifying B cells with varied interferon and antigen responsiveness in relation to each vaccine. This high-resolution dataset is amenable to further biomarker discovery and hypothesis generation.

immunology↗

bioRxiv2024

Small molecule FICD inhibitors suppress endogenous and pathologic FICD-mediated protein AMPylation

The AMP transferase, FICD, is an emerging drug target finetuning stress signaling in the endoplasmic reticulum (ER). FICD is a bi-functional enzyme, catalyzing both AMP addition (AMPylation) and removal (deAMPylation) from the ER resident chaperone BiP/GRP78. Despite increasing evidence linking excessive BiP/GRP78 AMPylation to human diseases, small molecules to inhibit pathogenic FICD variants are lacking. Using an in-vitro high-throughput screen, we identify two small-molecule FICD inhibitors, C22 and C73. Both molecules significantly inhibit FICD-mediated BiP/GRP78 AMPylation in intact cells while only weakly inhibiting BiP/GRP78 deAMPylation. C22 and C73 also efficiently inhibit pathogenic FICD variants and improve proinsulin processing in {beta} cells. Our study identifies and validates FICD inhibitors, highlighting a novel therapeutic avenue against pathologic protein AMPylation.

cell biology↗

bioRxiv2024

Ellagic acid: a potential inhibitor of enhancer of zeste homolog-2 and protein arginine methyltransferase-5

Dysregulation of epigenetic processes, characterized by aberrant DNA methylation patterns and histone modifications, is a hallmark of cancer, driving its initiation, progression, and metastasis by silencing tumor suppressor genes or activating oncogenes. Perturbations in histone modifications such as H3K27me3 by EZH2 and H4R3me2s by PRMT5 play significant roles in these epigenetic alterations, disrupting normal gene expression and facilitating oncogene activation while suppressing tumor suppressor genes. Consequently, inhibitors targeting enzymes involved in DNA methylation, histone modification, or chromatin remodeling, such as PRMTs and PRC complexes, are promising anti-cancer agents, with several undergoing pre-clinical and clinical trials. Our screening of a phytochemical library revealed ellagic acid as an effective inhibitor of both EZH2 and PRMT5. Ellagic acid interacts strongly with the EZH2 and PRMT5:MEP50 complex, binding to their active sites through {pi}-cation interactions and hydrogen bonds. Surface Plasmon Resonance study confirmed potent binding affinities of ellagic acid, with KD values of 3.28E-06 and 6.54E-05 for EZH2 and PRMT5:MEP50 respectively. In-vitro assays validated inhibitory effects on EZH2 and PRMT5:MEP50 by reducing the levels of their catalytic products H3K27me3 and H4R3me2s respectively and induction of autophagy and apoptosis. Further In-vivo studies using mouse xenografts further demonstrated significant tumor size reductions upon oral administration of ellagic acid, with decreased expression of the proliferative marker ki67 and histone repressive marks. Taken together we showed that inhibition of EZH2 and PRMT5:MEP50 by ellagic acid could be used to develop breast cancer therapeutic drug.

cancer biology↗

bioRxiv2024

CountASAP: A Lightweight, Easy to Use Python Package for Processing ASAPseq Data

Declining sequencing costs coupled with the increasing availability of easy-to-use kits for the isolation of DNA and RNA transcripts from single cells have driven a rapid proliferation of studies centered around genomic and transcriptomic data. Simultaneously, a wealth of new techniques have been developed that utilize single cell technologies to interrogate a broad range of cell-biological processes. One recently developed technique, transposase-accessible chromatin with sequencing (ATAC) with select antigen profiling by sequencing (ASAPseq), provides a combination of chromatin accessibility assessments with measurements of cell-surface marker expression levels. While software exists for the characterization of these datasets, there currently exists no tool explicitly designed to reformat ASAP surface marker FASTQ data into a count matrix which can then be used for these downstream analyses. To address this, we created CountASAP, an easy-to-use Python package purposefully designed to transform FASTQ files from ASAP experiments into count matrices compatible with commonly-used downstream bioinformatic analysis packages. CountASAP takes advantage of the independence of the relevant data structures to perform fully parallelized matches of each sequenced read to user-supplied input ASAP oligos and unique cell-identifier sequences.

bioinformatics↗

bioRxiv2024

Nerve injury downregulates δ-opioid and cannabinoid CB1 receptor genes through REST in primary sensory neurons

The transcription repressor REST in the dorsal root ganglion (DRG) is upregulated by peripheral nerve injury and promotes the development of chronic pain. However, the genes targeted by REST in neuropathic pain development remain unclear. The expression levels of 4 opioid receptor (Oprm1, Oprd1, Oprl1, Oprk1) and the cannabinoid CB1 receptor (Cnr1) genes in the DRG regulate nociception. In this study, we determined the role of REST in the control of their expression in the DRG induced by spared nerve injury (SNI) in both male and female mice. Transcriptomic analyses of male mouse DRGs followed by quantitative reverse transcription polymerase chain reaction analyses of both male and female mouse DRGs showed that SNI upregulated expression of Rest and downregulated mRNA levels of all 4 opioid receptor and Cnr1 genes, but Oprm1 was upregulated in female mice. Analysis of publicly available bioinformatic data suggested that REST binds to the promoter regions of Oprm1 and Cnr1. Chromatin immunoprecipitation analyses indicated differing levels of REST at these promoters in male and female mice. Full-length Rest conditional knockout in primary sensory neurons reduced SNI-induced pain hypersensitivity and rescued the SNI-induced reduction in the expression of Oprd1 and Cnr1 in the DRG in both male and female mice. Our results suggest that nerve injury represses the transcription of Oprd1 and Cnr1 via REST in primary sensory neurons and that REST is a potential therapeutic target for neuropathic pain.

neuroscience↗

bioRxiv2024

Epigallocatechin-3-gallate inhibit the protein arginine methyltransferase 5 and Enhancer of Zeste homolog 2 in breast cancer both in vitro and in vivo

Histone methyltransferases are selectively catalyzing the methylation of lysine or arginine residues of target histone and non-histone proteins, classified as lysine methyltransferases and arginine methyltransferases. The EZH2 and PRMT5 catalyze trimethylation of H3 at K27 and symmetric dimethylation of H4 at R3 respectively. These histone repressive marks have been considered as hallmarks in cancer. Both PRMT5 and EZH2 over expressed in several cancers and have been considered as important target of drug development. As a result, many synthetic molecules as inhibitors of both PRMT5 and EZH2 are at different level of preclinical and clinical phases. Cancer atlas data analysis revealed that both PRMT5 and EZH2 had shown more than 90% amplification in breast cancer alone. We screened an array of phytocompounds towards the inhibition of PRMT5 and EZH2 using in silico, in vitro assays. Among them Epigallocatechin-3-gallate (EGCG) has interacted with human PRMT5: MEP50 and EZH2 efficiently. The EGCG interacted within the SAM binding site, with a {pi}-cation interaction at Lys 333 and H-bonds with Tyr324, Tyr334, Gly365, Leu437, and Glu444. Surface plasmon resonance analysis revealed that EGCG has strong binding affinity in nanomolar concentrations with both PRMT5-MEP50 than EZH2. Further in vitro methylation and cell-based assays proved the inhibitory potential of EGCG by reducing the catalytic products of PRMT5 and EZH2 i.e., H4R3me2s & H3K27me3 respectively and showed that it induced autophagy and apoptosis. Furthermore in vivo, mouse xenografts studies demonstrated that oral dosage, reduced tumor size significantly with reduction in proliferation marker Ki67 and these histone repressive marks. Finally conclude that inhibition of PRMT5 and EZH2 by EGCG potentially can be used to develop combined therapeutic approaches.

cancer biology↗

bioRxiv2023

Epstein Barr virus infection induces tissue-resident memory T cells in mucosal lymphoid tissues

Epstein Barr virus (EBV) contributes to around 2% of all tumors worldwide. Simultaneously, more than 90% of healthy human adults persistently carry EBV without clinical symptoms. In most EBV carriers it is thought that virus-induced tumorigenesis is prevented by cell-mediated immunity. Specifically, memory CD8+ T cells recognize EBV-infected cells during latent and lytic infection. Using a symptomatic primary infection model, similar to infectious mononucleosis (IM), we found EBV induced CD8+ tissue resident memory T cells (TRMs) in mice with a humanized immune system. These human TRMs were preferentially established after intranasal EBV infection in nasal-associated lymphoid tissues (NALT), equivalent to tonsils, the primary site of EBV infection in humans. They expressed canonical TRM markers, including CD69, CD103 and BLIMP-1, as well as Granzyme B, CD107a and CCL5, while demonstrating reduced CD27 expression and proliferation by Ki-67 expression. Despite cytotoxic activity and cytokine production ex vivo, these TRMs failed to control EBV viral loads in the NALT during infection although effector memory T cells (TEMs) controlled viral titers in spleen and blood. Overall, TRMs in mucosal lymphoid tissues are established by EBV infection, but primarily systemic CD8+ T cell expansion seems to attenuate viral loads in the context of IM-like infection. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=160 SRC="FIGDIR/small/565960v1_ufig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@1cc2a9borg.highwire.dtl.DTLVardef@1013ea1org.highwire.dtl.DTLVardef@b6be98org.highwire.dtl.DTLVardef@19af7c7_HPS_FORMAT_FIGEXP M_FIG C_FIG

immunology↗

bioRxiv2022

Bi-Phasic Quasistatic Brain Communication for Fully Untethered Connected Brain Implants

Wireless communication using electro-magnetic (EM) fields acts as the backbone for information exchange among wearable devices around the human body. However, for Implanted devices, EM fields incur high amount of absorption in the tissue, while alternative modes of transmission including ultrasound, optical and magnetoelectric methods result in large amount of transduction losses due to conversion of one form of energy to another, thereby increasing the overall end-to-end energy loss. To solve the challenge of wireless powering and communication in a brain implant with low end-end channel loss, we present Bi-Phasic Quasistatic Brain Communication (BP-QBC), achieving < 60dB worst-case end-to-end channel loss at a channel length of ~55mm, by using Electro-quasistatic (EQS) Signaling that avoids transduction losses due to no field-modality conversion. BP-QBC utilizes dipole coupling based signal transmission within the brain tissue using differential excitation in the transmitter (TX) and differential signal pick-up at the receiver (RX), while offering ~41X lower power w.r.t. traditional Galvanic Human Body Communication (G-HBC) at a carrier frequency of 1MHz, by blocking any DC current paths through the brain tissue. Since the electrical signal transfer through the human tissue is electro-quasistatic up to several 10s of MHz range, BP-QBC allows a scalable (bps-10Mbps) duty-cycled uplink (UL) from the implant to an external wearable. The power consumption in the BP-QBC TX is only 0.52 W at 1Mbps (with 1% duty cycling), which is within the range of harvested power in the downlink (DL) from a wearable hub to an implant through the EQS brain channel, with externally applied electric currents < 1/5th of ICNIRP safety limits. Furthermore, BP-QBC eliminates the need for sub-cranial interrogators/repeaters, as it offers better signal strength due to no field transduction. Such low end-to-end channel loss with high data rates enabled by a completely new modality of brain communication and powering has deep societal and scientific impact in the fields of neurobiological research, brain-machine interfaces, electroceuticals and connected healthcare.

biophysics↗

bioRxiv2020

Bio-Physical Modeling of Galvanic Human Body Communication in Electro-Quasistatic Regime

Human Body Communication (HBC) is an alternative to radio wave-based Wireless Body Area Network (WBAN) because of its low-loss, wide bandwidth leading to enhanced energy efficiency. HBC also shows better performance in terms of physical security as most of the signal is confined within the body. To obtain optimum performance and usability, modeling of the body channel plays a vital role. Out of two HBC modalities, Galvanic HBC has the promise to provide lower loss compare to Capacitive HBC for shorter channel length. In this paper, we present the first lumped element based detailed model of Galvanic HBC channel which is used to explain the dependency of channel loss on the material property of skin, fat and muscle tissue layer along with electrode size, electrode separation, geometrical position of the electrodes and return path capacitance. The model considers the impedance of skin and muscle tissue layers and the effect of various coupling capacitances between the body and Tx/Rx electrodes to the Earth-ground. A 2D planner structure is simulated in HFSS to prove the validity of the proposed model. The effect of symmetry and asymmetry at the transmitter and receiver end are also explained using the model. The experimental results show that, due to the mismatch at the transmitter and receiver side, the loss increases gradually with channel length and saturates to a finite value as channel length becomes significantly longer compare to the transmitting or receiving electrode pair separation.

bioengineering↗