Biology subjects

Mercer, T.

Publications and source records attributed to Mercer, T..

5 recordsLinked to original sources

bioRxiv2026

SNR Enhancement Considerations for Loop Receive Coils at Ultra-High Fields

PurposeTo quantify parasitic losses in ultra-high field (UHF) magnetic resonance imaging (MRI) receive coils and determine how they contribute to the mismatch between numerically predicted and experimentally realized signal-to-noise ratio (SNR), with the goal of guiding receive-array designs toward ultimate intrinsic SNR (uiSNR). MethodsSNR was measured across multiple field strengths (3T, 7T, 10.5T) using commercial and custom-built arrays. To quantify parasitic losses, unloaded-to-loaded quality factor ratio (QR) measurements were performed on representative loop resonators and practical RF coils. Measured losses were combined with single-loop electromagnetic simulations to separate conductor, radiation, and component losses. These bench-derived loss estimates were then incorporated into full-array electromagnetic simulations of a 128-channel receive array to evaluate their impact on predicted intrinsic SNR. ResultsMeasurements across field strengths supported the expected supralinear increase of SNR with B0. QR analysis showed that, at UHF, radiation loss must be excluded from unloaded-Q measurements to avoid overestimating electronic-noise penalties, and that multiple seemingly modest parasitic losses collectively impose substantial SNR degradation. In the 128-channel array, simulations including only conductor and radiation losses predicted 93% of central uiSNR, whereas inclusion of the full measured parasitic-loss budget reduced predicted performance to 78%, in close agreement with the experimentally measured 77%. ConclusionsThe gap between predicted and realized SNR performance of high-channel-count 10.5T loop arrays can be largely explained by parasitic losses that are not captured in conventional simulations. A bench-measurement-informed simulation framework enables more realistic prediction of coil performance and provides practical guidance for optimizing future UHF receive arrays.

bioengineering↗

bioRxiv2026

An 80-channel receive array for 10.5T neuroimaging: Key considerations for SNR optimization

PurposeHigh-density RF receive arrays are required to realize the inherently available SNR and parallel imaging advantages at ultrahigh field strengths, which are essential for high-resolution functional and anatomical brain MRI. This study aims to systematically assess the impacts of often-overlooked parasitic losses associated with various RF coil components, as these losses can degrade the realized SNR and cause significant deviation from the ultimate intrinsic SNR (uiSNR; the theoretical upper bound of available SNR). In addition, we seek to detail engineering solutions to each of these loss mechanisms in pursuit of achieving a higher fraction of the uiSNR limit. MethodsA 16-channel loop-folded dipole transceiver array was developed for 10.5T human head applications and paired with a fully-updated 64-channel receive-only loop array. The optimization of the receive array considered several factors, including (but not limited to) coil dimensions to accommodate a larger population, the size and number of loops to enhance SNR and parallel imaging performance, and circuit design strategies to minimize parasitic losses. The SNR and parallel imaging performance of the receive array were quantitatively assessed by comparison with the uiSNR, as well as existing high-channel-count receive arrays at 7T and 10.5T. Finally, the complete 16-channel transmit, 80-channel receive coil array was safety validated for human use and employed for high-resolution functional and anatomical MRI at 10.5T. ResultsInitial results show that the 80-channel array, featuring larger loops in an overlapped layout with optimized circuitry, significantly improves the SNR and approaches the uiSNR limit in a large fraction of the head, while maintaining or enhancing the parallel imaging performance compared to previously used non-overlap layout. ConclusionThis study suggests that, although the traditionally used high-channel-count loop receive array technology can approach the uiSNR limit in the >10T regime, meticulous design optimization--including systematic assessment and minimization of parasitic losses--has become increasingly critical for achieving this goal in this new field-strength territory.

neuroscience↗

bioRxiv2021

On the discovery of ADRAM, an experience-dependent long noncoding RNA that drives fear extinction through a direct interaction with the chaperone protein 14-3-3

Long-noncoding RNA (lncRNA) comprise a new class of genes that have been assigned key roles in development and disease. Many lncRNAs are specifically transcribed in the brain where they regulate the expression of protein-coding genes that underpin neuronal function; however, their role in learning and memory remains largely unexplored. We used RNA Capture-Seq to identify a large population of lncRNAs that are expressed in the infralimbic cortex of adult male mice in response to fear-related learning, with 14.5% of these annotated in the GENCODE database as lncRNAs with no known function. We combined these data with cell-type-specific ATAC-seq on neurons that had been selectively activated by fear-extinction learning, and revealed 434 lncRNAs derived from enhancer regions in the vicinity of protein-coding genes. In particular, we discovered an experience-induced lncRNA called ADRAM that acts as both a scaffold and a combinatorial guide to recruit the brain-enriched chaperone protein 14-3-3 to the promoter of the memory-associated immediate early gene Nr4a2. This leads to the expulsion of histone deactylases 3 and 4, and the recruitment of the histone acetyltransferase creb binding protein, which drives learning-induced Nr4a2 expression. Knockdown of ADRAM disrupts this interaction, blocks the expression of Nr4a2, and ultimately impairs the formation of fear-extinction memory. This study expands the lexicon of experience-dependent lncRNA activity in the brain, highlights enhancer-derived RNAs (eRNAs) as key players in the epigenetic regulation of gene expression associated with fear extinction, and suggests eRNAs, such as ADRAM, may constitute viable targets in developing novel treatments for fear-related anxiety disorders.

neuroscience↗

bioRxiv2021

Advancing quality-control for NGS measurement of actionable mutations in circulating tumor DNA

The primary objective of the FDA-led Sequencing and Quality Control Phase 2 (SEQC2) project is to develop standard analysis protocols and quality control metrics for use in DNA testing to enhance scientific research and precision medicine. This study reports a targeted next generation sequencing (NGS) method that enables more accurate detection of actionable mutations in circulating tumor DNA (ctDNA) clinical specimens. This advancement was enabled by designing a synthetic internal standard spike-in for each actionable mutation target, suitable for use in NGS following hybrid-capture enrichment and unique molecular index (UMI) or non-UMI library preparation. When mixed with contrived ctDNA reference samples, internal standards enabled calculation of technical error rate, limit of blank, and limit of detection for each variant at each nucleotide position, in each sample. True positive mutations with variant allele fraction too low for detection by current practice were detected with this method, thereby increasing sensitivity.

genomics↗

bioRxiv2020

Atlas and developmental dynamics of mouse DNase I hypersensitive sites

Early mammalian development is orchestrated by genome-encoded regulatory elements populated by a changing complement of regulatory factors, creating a dynamic chromatin landscape. To define the spatiotemporal organization of regulatory DNA landscapes during mouse development and maturation, we generated nucleotide-resolution DNA accessibility maps from 15 tissues sampled at 9 intervals spanning post-conception day 9.5 through early adult, and integrated these with 41 adult-stage DNase-seq profiles to create a global atlas of mouse regulatory DNA. Collectively, we delineated >1.8 million DNase I hypersensitive sites (DHSs), with the vast majority displaying temporal and tissue-selective patterning. Here we show that tissue regulatory DNA compartments show sharp embryonic-to-fetal transitions characterized by wholesale turnover of DHSs and progressive domination by a diminishing number of transcription factors. We show further that aligning mouse and human fetal development on a regulatory axis exposes disease-associated variation enriched in early intervals lacking human samples. Our results provide an expansive new resource for decoding mammalian developmental regulatory programs.

genomics↗