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Bao, S.

Publications and source records attributed to Bao, S..

At least 19 recordsLinked to original sources

Facilitating Valid Statistical Inference in Biomedical Image Synthesis

Generative AI for medical image synthesis is increasingly used to impute missing data and augment biomedical datasets. Yet despite achieving high computational similarity to their real-world counterparts, synthetic images remain uncommon in clinical research practice, in part because of concerns about their biological validity. Here, we evaluate whether synthetic images support reliable downstream statistical analysis and biological inference in magnetic resonance imaging (MRI) and multiplexed immunofluorescence (mIF) imaging. We find that associations between patient phenotypes and synthesized images can be severely attenuated. This is because synthesis methods typically omit clinically relevant covariates and therefore generate images that, although visually realistic, mask key biological differences. Furthermore, naive analyses treat synthesized images as if they were observed, ignoring the statistical uncertainty introduced by synthesis. Drawing on multiple imputation theory, we introduce Phenotype Aware Multiple Synthesis (PAMS), an analysis framework that requires no model retraining and instead adjusts synthesized output to recover valid biological estimates with appropriately calibrated uncertainty. Applied to MRI and mIF data, PAMS reduced estimation bias and restored nominal confidence interval coverage. Because it is compatible with existing synthesis pipelines, PAMS offers a practical and rigorous route to statistically and biologically valid use of synthesized images in biomedical imaging research.

bioinformatics↗

Decoding Spatial Programs in Human Glioblastoma Through Surprisal Information-Theoretical Analysis

Glioblastoma (GBM) is a highly heterogeneous and invasive brain tumor in which complex interactions among tumor cells, immune cells, and neurons shape disease progression and therapeutic resistance. Resolving spatial patterns programs in glioblastoma (GBM) requires analytical approaches that go beyond variance-driven embeddings. Here, we applied thermodynamic surprisal analysis, an information-theoretic decomposition framework, to spatial transcriptomic sequencing from human GBM specimens to identify orthogonal constraint modes that capture dominant and previously hidden spatial programs. Surprisal analysis revealed structured patterns in the data that are not highlighted by standard approaches such as PCA or cell type deconvolution, including immune-activation-associated signatures as well as spatial programs consistent with synapse remodeling. Coupling surprisal decomposition with spatial ligand-receptor interaction analysis, NICHES, along with multiplexed protein imaging connected these spatial hidden modes to reveal potential communication networks. Together, these results position surprisal analysis as a powerful, complementary strategy for interrogating spatial tumor architecture, enabling discovery of non-obvious spatial programs and interactions that are obscured by variance-based methods.

systems biology↗

Architectural Confinement and Seasonal Forcing Shape Cross-Domain Pathogen Assemblages in Complex Built Environments

Airborne microbial pathogens in built environments (BEs) may pose potential health threats, yet the ecological mechanisms governing their assembly and persistence across interconnected architectural spaces are less studied. Here, we conducted a year-long, multi-spatial investigation across a university campus complex, sampling the exhaust outlets of three indoor environments and the adjacent outdoor inlets. By integrating the 16S rRNA gene and ITS sequencing from 437 paired bacterial-fungal samples, we characterized the spatiotemporal dynamics of airborne opportunistic pathogen-containing genera. Our study showed that spatial filtering emerged as the dominant determinant of pathogen community structure, with confined elevator environments serving as reservoirs of pathogens with limited but continuous microbial influx from surrounding spaces. Superimposed on this spatial baseline, bacterial and fungal pathogens displayed distinct seasonal dynamics. Opportunistic fungal pathogens such as Fusarium peaked during autumn and winter, possibly driven by enhanced aerosol persistence and dispersal under cooler, drier conditions. In contrast, bacterial pathogens exhibited greater temporal resilience, with key taxa such as Listeria transcribed actively during winter, predisposing them to increased relative abundance during spring. Cross-domain ecological networks further revealed the dynamic interactions among pathogens, centered on the skeletal structure mediated by the keystone fungal pathogen Aspergillus, suggesting that coordinated microbial interactions reinforced pathogen persistence across seasons. Together, our findings support a unified ecological framework in which pathogen dynamics within BEs arise from the coupled effects of spatial filtering, climatic modulation, and biotic interactions. These results provide a foundation for transitioning from static environmental control toward predictive pathogen management in BEs. ImportanceBEs are the primary settings of human microbial exposure, yet the ecological principles governing the persistence of airborne pathogens across interconnected indoor spaces remain poorly resolved. Most previous indoor studies have focused on isolated environments or single microbial groups, limiting our understanding of how pathogens are maintained and redistributed within complex architectural systems. By integrating bacterial and fungal community dynamics across spatial environments over four seasons, this year-long study demonstrates that the ecology of airborne pathogens is not static, but is instead dictated by a complex interplay of spatial, climatic, and biological forces. Our findings identify enclosed, high-transit elevator spaces as critical hotspots for pathogen accumulation and highlight the role of seasonal ecological reorganization in driving airborne health risks. More broadly, this work establishes a systems-level ecological framework for understanding airborne pathogen dynamics in BEs and provides a conceptual basis for developing more adaptive strategies for indoor microbial risk management.

microbiology↗

The Ser83, Arg85, Tyr88, Asn124, Lys192 of C-terminal Lipid-associated membrane hemagglutinin affecting Mycoplasma synoviae agglutination of erythrocyte

Mycoplasma synoviae is an avian pathogen that causes respiratory disease and synovitis, and its hemagglutinin plays a critical role in host cell adhesion. However, the key residues and structural mechanisms underlying hemagglutination remain unclear. In this study, domain analysis of the hemagglutinin family of Mycoplasma synoviae revealed that it contains long-chain and short-chain types, among which LAM HA (VY93_RS01465) was selected as the bait protein due to its complete C-terminal conserved domain. Through yeast two-hybrid screening, 18 host proteins interacting with LAM HA were identified. Furthermore, five key amino acid residues S83, R85, Y88, N124, and K192 were found to mediate hemagglutination activity. Deletion of these residues reduced the hemagglutination titer of LAM HA under acidic conditions. Secondary structure analysis showed that the deletion mutation decreased the -helix content while increasing the proportions of {beta}-sheet and random coil. Molecular dynamics simulations revealed that the mutant exhibited generally higher root mean square deviation and root mean square fluctuation values than the wild-type under different pH conditions, with a marked decrease in structural stability particularly at pH 5.0 and 6.0. These findings indicate that LAM HA, as a critical adhesin, exerts its hemagglutination function dependent on specific key residues and pH-sensitive conformational stability. IMPORTANCEMycoplasma synoviae (M. synoviae) causes significant economic losses to the poultry industry worldwide. Lipid-related membrane protein hemagglutinin (LAM HA) is a surface adhesin essential for host cell attachment, but its precise amino acid residues and structural features have not been defined. In this study, five key residues (S83, R85, Y88, N124, and K192) were identified as critical for LAM HA-mediated hemagglutination activity. Deletion of these residues altered the secondary structure composition, reduced conformational stability under acidic pH conditions, and decreased hemagglutination activity. These findings reveal a previously unknown structure-function relationship of M. synoviae LAM HA, demonstrating that its hemagglutination activity depends on specific residues and pH-sensitive structural integrity. This provides new insights into the molecular mechanisms of M. synoviae adhesion and offers potential targets for the development of novel intervention strategies against avian mycoplasmosis.

microbiology↗

Multidimensional MRI reveals cellular-scale microstructural phenotypes in human brain aging

Brain aging is accompanied by profound cellular and microstructural changes that precede overt tissue loss, yet in vivo MRI studies largely emphasize macroscopic measures or isolated diffusion and relaxation metrics, providing limited insight into how cellular-scale tissue architecture is altered across the adult lifespan. Here, we apply multidimensional diffusion-relaxation MRI (MD-MRI) to map voxel-wise microstructural phenotypes in cognitively unimpaired adults spanning early adulthood to late life (23-77 years). Rather than relying on predefined compartment models, MD-MRI resolves continuous voxel-wise distributions in a joint diffusion-relaxation space, enabling an integrated, model-free description of how cellular shape, size, restriction, and chemical environment vary with age. Using this approach, we reveal age-related multilateral shifts within a complex microstructural landscape, marked by increasing heterogeneity and disorder across brain tissue. With age, cellular-scale features showed a systematic transition from small to larger length-scale structures accompanied by reduced microscopic restriction, indicating a loss of fine cellular barriers and expansion of extracellular space. In parallel, we show tissue-dependent alterations in fast-relaxing properties aligned with known gray- and white-matter aging processes, including iron accumulation and myelin loss. Together, these findings indicate that normative brain aging involves progressive reorganization of structure and composition at the cellular level, rather than uniform shifts in bulk tissue properties. By decoupling cellular-scale shape, size, restriction, and chemical environment in vivo, MD-MRI identifies increasing cellular heterogeneity and breakdown of microscopic restriction as central features of human brain aging and provides a biologically interpretable framework for linking microstructural reorganization to age-related functional decline.

neuroscience↗

In vivo-directed evolution identifies AAV-WM04 as a next-generation vector for potent and durable hearing restoration in DFNB9

Efficient and cell-specific gene delivery to cochlear inner hair cells (IHCs) remains a major challenge for inner ear gene therapy. Here, we identify and characterize a novel AAV2-derived capsid, AAV-WM04, that enables highly efficient and selective IHC transduction at low doses. Using an in vivo-directed evolution strategy, we generated a randomized AAV2 capsid library with 9-amino acid insertions and performed iterative selection in the adult mouse cochlea. Next-generation sequencing revealed enrichment of several variants, among which AAV-WM04 exhibited superior packaging efficiency and pronounced IHC tropism. AAV-WM04 achieved near-complete IHC transduction throughout the cochlear axis in adult mice, outperforming clinically relevant vectors with minimal off-target expression and no detectable ototoxicity. Robust and exclusive IHC transduction was further validated in non-human primates following round window membrane delivery, underscoring translational potential. Therapeutically, AAV-WM04 enabled efficient dual-AAV trans-splicing delivery of the large OTOF gene, resulting in uniform full-length otoferlin expression in IHCs. In a humanized Otof Q829X/Q829X mouse model, AAV-WM04 restored auditory function across a broad frequency range at relatively low doses and achieved durable hearing recovery. Collectively, these findings establish AAV-WM04 as a next-generation IHC-targeted vector with high efficiency, safety, and cross-species applicability for precision gene therapy of hereditary hearing loss.

genetics↗

SuperFocus enables whole-slide cell-level spatial omics from spot-based measurements and histology across modalities

Histopathology and molecular pathology are currently distinct diagnostic modalities for the most part, one revealing tissue morphology at cellular resolution and the other providing molecular measurements with limited or no spatial context. Projecting genome-scale molecular information onto histopathology images at single-cell resolution across whole tissue sections represents a long-sought goal for next-generation pathology. Here we present SuperFocus, a modality-agnostic computational platform that generates histopathology-integrated single-cell spatial multi-omics from spot-based spatial measurements acquired on the same or an adjacent section without requiring external reference data. SuperFocus combines constrained cascading imputation with feature-level and cell-level quality-control scores to reduce spurious predictions and quantify confidence. On a ground-truth spatial transcriptomics benchmark dataset, SuperFocus improves key accuracy metrics by 28-73% over existing methods. Across Patho-DBiT, spatial ATAC-RNA, spatial CITE-seq and Visium-MALDI-MSI (SMA) datasets, SuperFocus enables cell-resolved analyses of MALT lymphoma microenvironments, gene regulatory programs in human hippocampus, lipotoxic hepatocyte states in human MASH, and transcriptomic-metabolomic states linked to neurotransmission and neuroinflammation in Parkinsonian mouse brain. Overall, SuperFocus enables scalable whole-slide single-cell spatial multi-omics integrated with histopathology, bridging histology and genome-scale molecular profiling for next-generation molecular pathology.

bioinformatics↗

A Causal Role for the Hippocampus in Gating Rapid Motor Memory Consolidation

How humans acquire motor skills is a fundamental biological question. Early learning involves rapid gains during practice and brief rest, yet the causal contribution of the hippocampus remains unclear. Here, we applied individualized, MRI-guided transcranial ultrasound stimulation (TUS) to modulate the posterior hippocampus in healthy adults. To establish a physiological benchmark, we first showed that this TUS protocol produced a sustained reduction in corticospinal excitability when applied to the primary motor cortex. When applied to the posterior hippocampus, electroencephalography revealed reduced frontocentral gamma-band activity, providing physiological evidence of hippocampal-frontal network modulation. Behaviorally, TUS altered the temporal dynamics of skill acquisition. Compared with sham, hippocampal TUS attenuated micro-offline gains during rest while increasing performance improvements during active practice. This shift from offline to online learning was replicated in an independent cohort with comparable baseline motor performance. Importantly, hippocampal TUS enhanced overall performance during learning, and this higher level of performance remained evident 24 hours later. Together, these findings provide causal evidence that the human hippocampus contributes to how motor learning is distributed between active practice and brief rest, showing that this temporal organization of learning can be altered by non-invasive neuromodulation.

neuroscience↗

BASSL-MI: Batch-Agnostic Self-Supervised Learning Uncovers Clinically Relevant Tumor Niches in Multiplexed Imaging

Multiplexed imaging enables rich, high-resolution characterization of the tumor microenvironment but relies on labor-intensive and error-prone cell segmentation and phenotyping pipelines. We present BASSL-MI, a batch-agnostic, self-supervised framework for discovering tissue niches directly from multiplexed imaging data. BASSL-MI operates directly on image patches, eliminating the need for explicit cell segmentation while mitigating image-, sample-, or batch-specific artifacts. Built on a modified contrastive block disentanglement architecture, BASSL-MI learns dual latent representations that separate biologically informative features from batch-dependent factors through spatially guided augmentations and batch-invariance objectives. Applied to a 56-marker colorectal cancer CODEX dataset, BASSL-MI-trained embeddings markedly reduce image-specific variability and recover biologically interpretable spatial niches. Notably, it uncovers CD20-rich follicular regions associated with improved survival, outperforming published findings from cell segmentation-driven clustering. This work demonstrates that self-supervised, patch-based learning can capture clinically relevant spatial organization within tumor microenvironments, advancing toward automated, non-cell-based analysis of multiplexed imaging data.

bioinformatics↗

A CRISPR/Cas9-based system using dual-sgRNAs for efficient gene deletion in Mycobacterium abscessus

The increasing global prevalence of Mycobacterium abscessus infections presents a significant clinical challenge due to the pathogens intrinsic resistance to multiple antibiotics and poor treatment outcomes. Despite the necessity of genetic tools for studying its physiology, pathogenesis, and drug resistance, efficient methods for large-fragment deletions remain underdeveloped. Here, we report a CRISPR/Cas9-based dual-sgRNA system employing Streptococcus thermophilus CRISPR1-Cas9 (Sth1Cas9), enabling efficient large-fragment knockout in M. abscessus with deletion efficiencies exceeding 90% at certain loci and spanning up to 16.7 kb. Furthermore, we systematically optimized the modular arrangement of genetic components in Cas9/dual-sgRNA expression plasmids and refined their construction workflow, achieving a significant reduction in cassette loss rates while enabling single-step plasmid assembly. Notably, deletion efficiency was position-dependent rather than correlated with target size, suggesting an influence of chromatin structure on editing outcomes. As the first CRISPR/Cas9-based platform capable of kilobase-scale deletions in M. abscessus, this system advances functional genomics studies and facilitates targeted investigations into virulence and antibiotic resistance mechanisms.

microbiology↗

Spatial epigenomic niches underlie glioblastoma cell state plasticity

IDH-wildtype glioblastoma (GBM) is an aggressive brain tumor with poor survival and few therapeutic options. Transcriptionally-defined cell states coexist in GBM and occupy defined regions of the tumor. Evidence indicates that GBM cell states are plastic, but it remains unclear if they are determined by the underlying epigenetic state and/or by microenvironmental factors. Here, we present spatially-resolved epigenomic profiling of human GBM tissues that implicate chromatin structure as a key enabler of cell plasticity. We report two epigenetically-defined and spatially-nested tumor niches. Each niche activates short-range molecular signals to maintain its own state and, surprisingly, long-range signals to reinforce the state of the neighboring niche. The position of a cell along this gradient-like system of opposing signals determines its likelihood to be in one state or the other. Our results reveal an intrinsic system for cell plasticity that is encoded in the chromatin profiles of two adjacent niches that dot the topological architecture of GBM in cartesian space.

genomics↗

Variant Classification Using Proteomics-Informed Large Language Models Increases Power of Rare Variant Association Studies and Enhances Target Discovery

Rare variant association analysis, which assesses the aggregate effect of rare damaging variants within a gene, is a powerful strategy for advancing knowledge of human biology. Numerous models have been proposed to identify damaging coding variants, with the most recent ones employing deep learning and large language models (LLM) to predict the impact of changes in coding sequences. Here, we use newly available proteomics data on 2,898 proteins across 46, 665 individuals to evaluate and refine LLM predictors of damaging variants. Using one of these refined models, we evaluate association between rare damaging variants and human phenotypes at 241 positive control gene-trait pairs. Among these gene-trait pairs, our proteomics-guided model outperforms an ensemble of conventional approaches including PolyPhen2, Mutation Taster, SIFT, and LRT, as well as newer machine learning approaches for identifying damaging missense variants, such as CADD, ESM-1v, ESM-1b and AlphaMissense. When attempting to recover known associations by correctly separating damaging singleton missense variants from other singleton variants, our approach recapitulates 36.5% of gene-trait pairs with known associations, exceeding all the alternatives we considered. Furthermore, when we apply our model to 10 exemplary traits from the UK Biobank, we identify 177 gene-trait associations - again exceeding all other approaches. Our results demonstrate that summary statistics from large-scale human proteomics data enable evaluation and refinement of coding variant classification LLMs, improving discovery potential in human genetic studies.

bioinformatics↗

Changes in Motor Unit Activity of Co-activated Muscles During Dynamic Force Field Adaptation

Muscle co-contraction plays a critical role in motor adaptation by minimizing movement errors and enhancing joint stability in novel dynamic environments. However, the underlying changes in motor unit (MU) activity within co-activated muscles during adaptation remain largely unexplored. To investigate this, we employed advanced electromyography sensor arrays and signal processing to examine MU activation in the triceps brachii (agonist) and biceps brachii (antagonist) during a reaching task under force-field perturbation. Our results revealed a gradual reduction in movement errors and an increase in velocity with adaptation, accompanied by a decrease in muscle co-contraction from early to late adaptation phases. This reduction was primarily driven by increased triceps activity, while biceps activity remained unchanged throughout the adaptation process. At the MU level, recruitment, amplitude, and firing rate increased in both muscles during adaptation compared to baseline (without force-field perturbation). However, from early to late adaptation phases, triceps MU amplitude continued to increase, while its firing rate stabilized, suggesting a shift in force generation strategy. In contrast, biceps MU activity remained stable throughout the adaptation. These findings indicate that the reduction in co-contraction during motor adaptation is likely mediated by a shift in motor unit control strategy within the agonist muscle. The increased reliance on MU amplitude modulation rather than firing rate in later adaptation may represent a mechanism for optimizing force production while maintaining movement accuracy and joint stability in dynamic environments. NEW & NOTEWORTHYThis study examines how motor unit (MU) activity changes during motor adaptation in dynamic environments. We show that reduced co-contraction during adaptation is primarily driven by increased agonist MU amplitude rather than firing rate changes. In contrast, antagonist MU activity remains stable. These findings highlight a shift in MU control strategy that optimizes force production while maintaining movement accuracy, providing new insights into the underlying neuromuscular mechanisms of motor adaptation.

neuroscience↗

Cell type transcriptional identities are maintained in cultured ex vivo human brain tissue

It is becoming more broadly accepted that human-based models are needed to better understand the complexities of the human nervous system and its diseases. The recently developed human brain organotypic culture model is one highly promising model that requires the involvement of neurosurgeons and neurosurgical patients. Studies have investigated the electrophysiological properties of neurons in such ex vivo human tissues, but the maintenance of other cell types within explanted brain remains largely unknown. Here, using single-nucleus RNA sequencing, we systematically evaluate the transcriptional identities of the various cell types found in six patient samples after fourteen days in culture (83,501 nuclei from day 0 samples and 45,738 nuclei from day 14 samples). We used two pediatric temporal lobectomy samples, an adult frontal cortex sample, two IDH wild-type glioblastoma samples, and one medulloblastoma sample. We found remarkably high correlations of day 14 transcriptional identities to day 0 tissue, especially in tumor cells (r = 0.90 to 0.93), though microglia (r = 0.86), oligodendrocytes (r = 0.80), pericytes (r = 0.77), endothelial cells (r = 0.78), and fibroblasts (r = 0.76) showed strong preservation of their transcriptional profiles as well. Astrocytes and excitatory neurons showed more moderate preservation (r = 0.66 and 0.47, respectively). Because the main difficulty with organotypic brain cultures is the acquisition of human tissue, which is readily available to neurosurgeons, this model is easily accessible to neurosurgeon-scientists and neurosurgeons affiliated with research laboratories. Broad uptake of this more representative model should prompt advances in our understanding of many uniquely human diseases, lead to more reliable clinical trial performance, and ultimately yield better therapies for our patients.

neuroscience↗

Modulating Motor Cortex Plasticity via Cortical and Peripheral Somatosensory Stimulation

The interaction between the motor and somatosensory systems is essential for effective motor control, with evidence indicating that somatosensory stimulation influences the excitability of the primary motor cortex (M1). However, the mechanisms by which repetitive stimulation of both cortical and peripheral somatosensory systems affects M1 plasticity are not well understood. To investigate this, we examined the effects of continuous theta-burst stimulation (cTBS) applied to the primary somatosensory cortex (S1) and transcutaneous electrical nerve stimulation (TENS) of the median nerve on various measures of corticospinal excitability and M1 intracortical circuits. Specifically, we assessed motor-evoked potentials (MEPs), short-latency intracortical inhibition (SICI), intracortical facilitation (ICF), and short-latency afferent inhibition (SAI) before and after administering cTBS and TENS. Our results demonstrated that cTBS increased MEPs for at least 50 minutes, whereas TENS increased MEPs for 10 minutes. Neither cTBS nor TENS had an impact on SICI and ICF. However, cTBS decreased SAI, while TENS did not affect SAI. The sham procedures for both cTBS and TENS did not produce significant changes in MEPs, SICI, ICF, or SAI. These findings suggest that both cortical and peripheral somatosensory stimulation modulate corticospinal excitability, with the effects of cortical stimulation being more prolonged. Neither type of stimulation influences inhibitory and excitatory intracortical neural circuitry within M1. Notably, cortical somatosensory stimulation modulates the interaction between M1 and S1, whereas peripheral somatosensory stimulation does not. This study elucidates distinct mechanisms through which cortical and peripheral somatosensory stimulation influence M1 plasticity. NEW & NOTEWORTHYThis study identifies distinct mechanisms through which cortical and peripheral somatosensory stimulation influence motor cortex (M1) plasticity. Both continuous theta-burst stimulation (cTBS) of the primary somatosensory cortex (S1) and transcutaneous electrical nerve stimulation (TENS) of the median nerve enhance corticospinal excitability, with cTBS exhibiting longer-lasting effects. Importantly, cTBS, but not TENS, modulates the interaction between M1 and S1. These findings form the basis for developing targeted somatosensory interventions aimed at modulating motor function.

neuroscience↗

Spatially Resolved in vivo CRISPR Screen Sequencing via Perturb-DBiT

Perturb-seq enabled the profiling of transcriptional effects of genetic perturbations in single cells but lacks the ability to examine the impact on tissue environments. We present Perturb-DBiT for simultaneous co- sequencing of spatial transcriptome and guide RNAs (gRNAs) on the same tissue section for in vivo CRISPR screen with genome-scale gRNA libraries, offering a comprehensive understanding of how genetic modifications affect cellular behavior and tissue architecture. This platform supports a variety of delivery vectors, gRNA library sizes, and tissue preparations, along with two distinct gRNA capture methods, making it adaptable to a wide range of experimental setups. In applying Perturb-DBiT, we conducted un-biased knockouts of tens of genes or at genome-wide scale across three cancer models. We mapped all gRNAs in individual colonies and corresponding transcriptomes in a human cancer metastatic colonization model, revealing clonal dynamics and cooperation. We also examined the effect of genetic perturbation on the tumor immune microenvironment in an immune-competent syngeneic model, uncovering differential and synergistic perturbations in promoting immune infiltration or suppression in tumors. Perturb-DBiT allows for simultaneously evaluating the impact of each knockout on tumor initiation, development, metastasis, histopathology, and immune landscape. Ultimately, it not only broadens the scope of genetic inquiry, but also lays the groundwork for developing targeted therapeutic strategies.

genomics↗

Common AAV gene therapy vectors show indiscriminate transduction of living human brain cell types

The development of cell-type-specific gene therapy vectors for treating neurological diseases holds great promise, but has relied on animal models with limited translational utility. We have adapted an ex vivo organotypic model to evaluate adeno-associated virus (AAV) transduction properties in living slices of human brain tissue. Using fluorescent reporter expression and single-nucleus RNA sequencing, we found that common AAV vectors show broad transduction of normal cell types, with protein expression most apparent in astrocytes; this work introduces a pipeline for identifying and optimizing AAV gene therapy vectors in human brain samples.

bioengineering↗

Connectivity between supplementary motor complex and primary motor cortex: a dual-coil paired-pulse TMS study

In recent years, dual-coil paired-pulse transcranial magnetic stimulation (ppTMS) has garnered interest for its potential in elucidating neural circuit dynamics. In this study, the dual-coil ppTMS was utilized to assess the effective connectivity between the supplementary motor complex (SMC) and the primary motor cortex (M1) in humans. A robust facilitatory connection between the SMC and M1 was observed, manifested as a 19% increase in mean peak-to-peak motor-evoked potentials following preconditioning of SMC 7 ms prior to M1 stimulation. Importantly, the facilitatory influence of SMC only occurred when the preconditioning stimulation was administered 4 cm anterior to Cz but not when applied at 5-cm, 6-cm, or 7-cm distance. While previous work has focused on demonstrating important temporal dynamics for SMC-M1 plasticity, the present findings highlight a critical contribution of spatial specificity for modulation of SMC-M1 circuitry. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/610643v1_ufig1.gif" ALT="Figure 1"> View larger version (44K): org.highwire.dtl.DTLVardef@12fb447org.highwire.dtl.DTLVardef@e4bfacorg.highwire.dtl.DTLVardef@1e3d262org.highwire.dtl.DTLVardef@93984_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIThe conditioned stimulus induced larger MEPs compared to the unconditioned stimulus C_LIO_LIThe connectivity between SMC and M1 diminished when the SMC coil was moved forward C_LIO_LIFindings highlight the importance of spatial specificity for modulation of SMC-M1 circuitry C_LI

neuroscience↗