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Niu, Y.

Publications and source records attributed to Niu, Y..

At least 37 records · Page 2Linked to original sources

Social observation influences the trajectory of performance monitoring across trials: evidence from single-trial estimates of the ERN and CRN

The error-related negativity (ERN) and correct-related negativity (CRN) are event-related potentials (ERPs) that reflect performance monitoring following error and correct responses, respectively. Prior work demonstrates the ERN is sensitive to the motivational significance of errors, which increases under social observation. However, most studies testing how social observation impacts performance monitoring rely on trial-averaged ERPs, potentially obscuring meaningful fluctuations in ERN/CRN over time. Here, we had participants complete a Flanker task twice (social observation vs. alone) and employed mixed-effects modeling of single-trial ERPs to test if social observation impacts ERN/CRN trajectories over short (within blocks) or long (between blocks) timescales. We found that social observation selectively influenced ERN/CRN trajectories over short timescales: for blocks performed under social observation (but not alone), ERN magnitudes increased across trials and CRN magnitudes decreased. At longer timescales, ERN/CRN significantly decreased across all blocks, regardless of social observation and consistent with a vigilance decrement. To our knowledge, this is the first demonstration that social observation influences performance monitoring trajectories over short timescales. Results highlight the importance of analyzing ERN/CRN trajectories over relatively short timescales to fully characterize the impact of social observation on performance monitoring dynamics. These findings lay the groundwork for future investigation into whether social observation interacts with individual differences in motivation/affect to differentially impact performance monitoring dynamics.

neuroscience↗

Chemo-mechanotherapy of fibrosis: dynamic control of biological materials through tissue-architecture-dependent crosslink disruption

Extracellular matrix (ECM) stiffness drives cell fate, but tissues are nonlinear and difficult to modify chemically without harming patients. Here, we show that nonlinear mechanical responses of fibrous and porous tissues can be controlled by mechanically modulating crosslinks. Through integrated in vivo, in vitro, and computational approaches, we found that physiological dynamic stretching disrupts pathological advanced glycation end-product (AGE) crosslink-induced fibrogenesis in an architecture-dependent manner. This was effective in lung-like porous scaffolds but not in liver-like fibrous matrices, revealing a critical structure-property relationship. Computational and in vitro models established that this modulates cell-ECM feedback, and that controlling mechanical crosslinking modulates key nonlinearity of networked solids. This discovery inspired a non-invasive, "mechanotherapuetic" ventilation protocol, which reversed pulmonary fibrosis in mice by physically disrupting ECM pathological crosslinks. The therapeutic efficacy was further amplified when combined with pharmacological AGE inhibition. These findings establish design principles for dynamically reprogrammable biological materials and mechano-targeted therapies.

bioengineering↗

Developmental changes in the carotid body transcriptome accompanying the maturation of chemosensitivity

The carotid body (CB) chemoreceptors mediate rapid cardiorespiratory reflexes to hypoxia, which mature peri-natally and are vital for fetal hypoxia tolerance and post-natal ventilatory control. This maturation is associated with an increase in the sensitivity of the CB electrophysiological response to hypoxia (chemosensitivity): a process that is incompletely understood but critical to systemic oxygen homeostasis. Hypothesizing that perinatal CB gene expression changes would reveal candidate mechanisms for oxygen chemosensitivity, we studied the CB transcriptome in sheep, where peri-natal CB physiology is well-characterised. CB-mediated cardiovascular reflexes are detectable at fetal day 120, and robust by term (day 145), while hypoxic ventilatory responses are established by post-natal day 15. We performed RNA sequencing on sheep CBs at each of these stages, and adults, along with the superior cervical ganglion (SCG) as an oxygen-insensitive control. This allowed us to define tissue-specific changes in the CB transcriptome correlating with chemosensitivity maturation. Striking, progressive CB enrichment is observed in genes implicated in murine CB chemosensitivity, including potassium channels (KCNK9), mitochondrial complex IV regulators (NDUFA4L2, HIGD1C), and HIF-2 (EPAS1). Genes with this expression pattern are also enriched for regulators of diacylglycerol (DAG), particularly the DAG kinase DGKH: one of the most abundant CB transcripts increasing in parallel with chemosensitivity. Across developmental stages, the CB also exhibits marked down-regulation of metabolic pathways and ATP/GTP consuming processes, potentially providing a state permissive to metabolic signal detection. Together, this builds a detailed picture of the CB transcriptional signature, with core features established in fetal life and conserved across species. Key pointsO_LIThe carotid body (CB) chemoreceptors mediate rapid cardiorespiratory responses to hypoxia, which maintain systemic oxygen homeostasis, but CB dysfunction is also implicated in pathologies including hypertension, heart failure and sudden infant death. C_LIO_LICB-mediated chemoreflexes mature during the peri-natal period, with increasing sensitivity of the oxygen chemosensory response. C_LIO_LIWe performed RNA-seq of CBs from sheep across 3 peri-natal stages and adults, enabling us to identify gene expression changes that correlate with functional state. C_LIO_LIWe describe a CB transcriptomic signature that is conserved across species, established in fetal life, and correlates with maturation. This includes features of a unique metabolic phenotype, and up-regulation of genes encoding the extracellular matrix and diacylglycerol signalling. The top transcription factor correlating with functional maturation is EPAS1/ HIF-2. C_LIO_LIWe anticipate that this data set will be a valuable resource in generating novel hypotheses on mechanisms of oxygen chemosensory function, development and CB-associated pathologies. C_LI

physiology↗

Single-nucleotide Resolution Epitranscriptomic Profiling Uncovers Dynamic m6A Regulation in Bovine Preimplantation Development

RNA N6-methyladenosine (m6A) plays a crucial role in regulating gene expression during early embryonic development. However, the m6A dynamics at single-nucleotide resolution in preimplantation development remain uncharacterized, and the functional significance of site specific m6A modifications in key developmental regulators is largely unknown. Here, using SAC-seq, a single-base resolution, antibody-independent m6A profiling method, we generate the first comprehensive m6A landscape in bovine oocytes and preimplantation embryos. We identify a previously uncharacterized m6A site in RPL12 transcript that is essential for embryonic development. Loss of m6A at this site leads to reduced protein synthesis, disrupted expression of translation-related genes, and impaired zygotic genome activation and blastocyst formation. Notably, supplementation with wild-type RPL12 mRNA fails to rescue the developmental arrest, indicating that m6A regulation extends beyond transcript abundance. Our findings provide a valuable resource of m6A at single-nucleotide resolution in mammalian embryogenesis and uncover a critical mechanism by which precise, site-specific m6A regulates translation and developmental competence in early embryos.

developmental biology↗

Mitochondrial Genome Variants and Nuclear Mitochondrial DNA Segments in 7331 Individuals from NyuWa and 1KGP

Dysfunctional mitochondria are implicated in various diseases, while little is known about comprehensive characterization of mitochondrial DNA (mtDNA) in Chinese population. Here, we conducted a systematic analysis of mtDNA from 7331 samples, comprising 4129 Chinese samples (NyuWa) and 3202 samples from the 1000 Genomes Project (1KGP). We identified 7216 distinct high-quality mtDNA variants and classified them into 22 macrohaplogroups, and detected 1466 distinct nuclear mitochondrial DNA segments (NUMTs), with 88 mtDNA variants and 642 NUMTs being specific to NyuWa. The genome-wide association analyses revealed that 12 mtDNA variants were significantly correlated with 199 nuclear DNA variants. Our findings revealed that all individuals in both NyuWa and 1KGP harbored common NUMTs, and one-fifth possessed ultra-rare NUMTs, which tended to insert into nuclear gene regions. Compared to 1KGP, significant enrichment of nuclear breakpoints in long interspersed nuclear elements (LINEs) was observed for rare NUMTs in NyuWa. Overall, this study represents the first comprehensive profiling the landscape of Chinese NUMTs and offers the most extensive resource of Chinese mtDNA variants and NUMTs based on high-depth WGS to date, providing valuable reference resources for genetic research on mtDNA-related diseases.

genomics↗

White matter microstructure and macrostructure brain charts across the human lifespan

Normative reference charts are widely used in healthcare, especially for assessing the development of individuals by benchmarking anatomic and physiological features against population trajectories across the lifespan. Recent work has extended this concept to gray matter morphology in the brain, but no such reference framework currently exists for white matter (WM) even though WM constitutes the essential substrate for neuronal communication and large-scale network integration. Here, we present the first comprehensive WM brain charts, which describe how microstructural and macrostructural features of WM evolve across the lifespan, by leveraging over 35,120 diffusion MRI scans from 50 harmonized studies. Using generalized additive models for location, scale, and shape (GAMLSS), we estimate age- and sex-stratified trajectories for 72 individual white matter pathways, quantifying both tract-specific microstructural and morphometric features. We demonstrate that these WM brain charts enable four important applications: (1) defining normative trajectories of WM maturation and decline across distinct pathways, (2) identifying previously uncharacterized developmental milestones and spatial gradients of tract maturation, (3) detecting individualized deviations from normative patterns with clinical relevance across multiple neurological disorders, and (4) facilitating standardized, cross-study centile scoring of new datasets. By establishing a unified, interpretable reference framework for WM structure, these brain charts provide a foundational metric for research and clinical neuroscience. The accompanying open-access trajectories, centile scoring tools, and harmonization methods facilitate precise mapping of WM development, aging, and pathology across diverse populations. We release the brain charts and provide an out-of-sample alignment process as a Docker image: https://zenodo.org/records/17561821.

neuroscience↗

A heart releasing neuropeptide that synchronizes brain-heart regulation during courtship behavior

Distinct internal states drive varied animal behaviors, yet the mechanisms by which non-neuronal factors encode these states remain largely unknown. Here, we show that cardiac activity regulates internal mating states through a conserved brain-heart axis in male flies and mice. In Drosophila, a ppk23-P1 pathway triggers heart rate acceleration upon female perception via crustacean cardioactive peptide, while the heart secretes ion transport peptide that feeds back onto P1 neurons to enhance courtship. Ejaculation rapidly decreases heart rate via Corazonin, mitigating prolonged tachycardia. In mice, a conserved Substance P-TacR1 pathway modulates courtship. Finally, we developed a computational framework to decode internal mating states from cardiac physiology, revealing distinct cardiac signatures. Our findings unveil a novel role for heart-derived neuropeptides in internal state regulation, elucidate a positive feedback loop between the heart and brain, and demonstrate the evolutionary conservation of the brain-heart axis in orchestrating dynamic behavioral and physiological states.

neuroscience↗

Constitutive and regulatory responses of Arabidopsis thaliana to harmonically oscillating light

The rate of net CO2 uptake is proportional to dim light and saturates when the light exceeds the plant assimilation capacity. This simple relationship between constant light and photosynthesis becomes intriguingly complex when the light oscillates. The rates of photosynthesis may differ between the descending and ascending phases of light oscillation. This hysteresis changes with the frequency and amplitude of the light and reports on the dynamics of the photosynthetic reactions and their regulation. Here, we investigated the chlorophyll fluorescence response of Arabidopsis thaliana to light oscillating with three different amplitudes: 100-200, 100-400, and 100-800 mol photons{middle dot}m-2{middle dot}s-1, each with periods ranging from 1 s to 8 min. The light amplitudes and periods were chosen to represent light patterns often appearing in nature. Three genotypes were compared: wild-type Col-0 and npq1 and npq4 mutants that are incapacitated in the rapidly reversible energy-dependent non-photochemical quenching (qE). The experiments identified two major dynamic patterns. One was found in oscillation periods shorter than 30 s, characterized by constitutive non-linearity and hysteresis. The other was mainly formed by regulatory non-linearity and hysteresis, occurring when the oscillation periods were longer than 30 s. The mathematical model simulating the chlorophyll fluorescence dynamics qualitatively reproduced the constitutive and regulatory dynamic patterns observed in the experiments. The model simulations illustrated the dynamics of non-photochemical quencher activation, plastoquinone pool reduction, and lumen pH that form the constitutive and regulatory non-linearities. The model simulations provided mechanistic insight into molecular processes forming the plant response to oscillating light.

plant biology↗

Multi-purpose controllable protein generation via prompted language models

Deep learning is increasingly powerful for designing proteins that meet structural and functional requirements. However, most existing methods follow a conventional pipeline: first defining a backbone structure and then generating sequences consistent with it. This approach, which encodes all design goals indirectly through structures, restricts flexibility and struggles to address multiple, complex design objectives simultaneously. We present PROPEND, a multi-purpose protein sequence design method based on the "pre-train and prompt" framework. We show PROPENDs broad utility and accuracy both in silico and in vitro by directly controlling multiple properties through the prompt of backbones, blueprints, functional tags, and their combinations. For the five sequences tested with in vitro experiments, PROPEND achieved a maximum functional recovery of 105.2%, significantly outperforming the classical design pipelines 50.8%.

synthetic biology↗

A Multi-Property Optimizing Generative Adversarial Network for de novo Antimicrobial Peptide Design

Antimicrobial peptides (AMPs) play a crucial role in developing novel antiinfective drugs due to their broad-spectrum antimicrobial activity and lower likelihood of causing bacterial resistance. However, laboratory synthesis of AMPs is tedious and time-consuming. Existing computational methods have limited capability in optimizing multiple desired properties simultaneously. Here, we propose a Multi-Property Optimizing Generative Adversarial Network (MPOGAN), a feedback-loop framework that iteratively learns from data with multiple desired properties. This approach enables de novo design of AMPs with potent antimicrobial activity, reduced cytotoxicity, and diversity. Through extensive computational tests, MPOGAN exhibits superior performance in optimizing multiple desired properties of generated AMPs. Ten of the most promising candidates are chemically synthesized, with nine showing potent antimicrobial activity against three bacterial strains and low cytotoxicity against eukaryotic cells. MPOGAN offers a powerful computational approach for effective multi-property optimization of AMPs, thereby advancing the field of AI-aided drug discovery.

bioinformatics↗

Cross-Species Analysis Reveals No Universal Programmed Aging Mechanism: Insights from Single-Cell Transcriptomics in Zebrafish, Fruit Fly, and Nematode

The question of whether aging follows a universal programmed process has been a topic of debate for a long time. Previous arguments, either supporting or refuting programmed aging, were mainly based on different evolutionary biology theories. In this study, we analysed single-cell RNA sequencing data from zebrafish, fruit fly, and nematode at various stages of development to explore gene co-expression modules across these species. We successfully identified a co-expression module related to ribosomal protein genes that is shared across the early development stages in multiple tissues of all three species. However, we did not find any cross-species shared gene co-expression modules related to aging. Further analysis of gene regulatory networks (GRNs) demonstrated that although certain aging-related genes are conserved, their regulatory mechanisms vary significantly between species. These findings suggest that aging is not governed by a conserved universal program but rather by species-specific adaptations to damage and environmental conditions.

evolutionary biology↗

Flanker task parameters are related to the strength of association between the ERN and anxiety: a meta-analysis

The error-related negativity (ERN)--an index of error monitoring--is associated with anxiety symptomatology. Although recent work suggests associations between the ERN and anxiety are relatively modest, little attention has been paid to how variation in task parameters may influence the strength of ERN-anxiety associations. To close this gap, the current meta-analysis assesses the possible influence of task parameter variation in the Flanker task--the most commonly used task to elicit the ERN--on observed ERN-anxiety associations. Here, we leveraged an existing open database of published/unpublished ERN-anxiety effect sizes, supplementing this database by further coding for variation in stimulus type (letter vs. arrow), response type (one-handed vs. two-handed), and block-level feedback (with vs. without). We then performed meta-regression analyses to assess whether variation in these Flanker task parameters moderated the effect size of ERN-anxiety associations. No evidence for an effect of stimulus type was identified. However, both response type and block-level feedback significantly moderated the magnitude of ERN-anxiety associations. Specifically, studies employing either a two-handed (vs. one-handed) task, or those with (vs. without) block-level feedback exhibited more than a two-fold increase in the estimated ERN-anxiety effect size. Thus, accounting for common variation in task parameters may at least partially explain apparent inconsistencies in the literature regarding the magnitude of ERN-anxiety associations. At a practical level, these data can inform the design of studies seeking to maximize ERN-anxiety associations. At a theoretical level, the results also inform testable hypotheses regarding the exact nature of the association between the ERN and anxiety.

neuroscience↗

Targeting PRMT3 Impairs Methylation and Oligomerization of HSP60 to Boost Anti-Tumor Immunity by Activating cGAS/STING Signaling

Hepatocellular carcinoma (HCC) is a highly lethal cancer for which current available treatment options have limited efficacy. Immunotherapy has emerged as a promising therapeutic option for HCC, yet resistance to immunotherapy is a major challenge. Here, we uncover protein arginine methyltransferase 3 (PRMT3) as a novel driver of immunotherapy resistance in HCC. We show that PRMT3 expression is induced by activated T cells in response to immune checkpoint blockade (ICB) via an interferon-gamma (IFN{gamma})-STAT1 signaling pathway, and that high PRMT3 expression inversely correlates with tumor-infiltrating CD8+ T cells and predicts poor response to ICB in HCC patients. We demonstrate that genetic depletion and pharmacological inhibition of PRMT3 induce a profound influx of T cells into tumors and activate anti-tumor immunity to suppress HCC progression. Mechanistically, we demonstrate that PRMT3 methylates HSP60, a mitochondrial chaperone protein, at R446, and that this novel post-translational modification is required for HSP60 oligomerization and maintaining mitochondrial homeostasis. We reveal that targeting PRMT3-dependent HSP60-R446 methylation boosts anti-tumor immunity by disrupting mitochondrial function, increasing mitochondrial DNA (mtDNA) leakage, and activating the cGAS/STING pathway, a key innate immune sensor of cytosolic DNA. Importantly, we provide genetic and pharmacologic evidence that targeting PRMT3 enhances anti-PD1 efficacy and anti-tumor immunity in HCC mouse models. Our study identifies PRMT3 as a potential biomarker and therapeutic target to overcome immunotherapy resistance in HCC.

cancer biology↗

hESCs-derived organoids achieve liver zonation by LSEC modulation

Liver zonation, essential for diverse physiological functions, is lacking in existing organoid models, hindering their ability to recapitulate liver development and pathogenesis. Addressing this gap, we explored the feasibility of achieving zonated organoid by co-culturing human embryonic stem cells (hESCs) derived hepatocytes with hESCs derived liver sinusoidal endothelial cells (LSECs) exhibiting characteristics of either the liver lobules pericentral (PC) or periportal (PP) regions. Introducing zonated LSECs with variable WNT2 signaling subtly regulate hepatocyte zonation, resulting in noticeable metabolic function changes. Considering the lipid metabolism variations in PC and PP organoids, we constructed biomimetic zonated non-alcoholic fatty liver disease (NAFLD) organoids and revealed that glucagon-like peptide-1 receptor agonist (GLP-1RA) target LSECs, but not hepatocytes, indicating potential therapeutic mechanisms of GLP-1RA in NAFLD alleviation. This study highlights the crucial role of non-parenchymal cells in organoids for recapitulating niche heterogeneity, offering further insights for drug discovery and in vitro modeling of organ heterogeneity. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=184 SRC="FIGDIR/small/592562v1_figu1.gif" ALT="Figure 1"> View larger version (57K): org.highwire.dtl.DTLVardef@1907c9eorg.highwire.dtl.DTLVardef@e5a76borg.highwire.dtl.DTLVardef@152a1dcorg.highwire.dtl.DTLVardef@981f_HPS_FORMAT_FIGEXP M_FIG Graphical AbstractSchematic of hESCs-derived liver zonation organoids C_FIG

bioengineering↗

Distinct effects of CDK8 module subunits on cellular growth and proliferation in Drosophila

The Mediator complex, composed of about 30 conserved subunits, plays a pivotal role in facilitating RNA polymerase II-dependent transcription in eukaryotes. Within this complex, the CDK8 kinase module (CKM), comprising Med12, Med13, CDK8, and CycC (Cyclin C), serves as a dissociable subcomplex that modulates the activity of the small Mediator complex. Genetic studies in Drosophila have revealed distinct phenotypes of CDK8-CycC and Med12-Med13 mutations, yet the underlying mechanism has remained unknown. Here, using Drosophila as a model organism, we show that depleting CDK8-CycC enhances E2F1 target gene expression and promotes cell-cycle progression. Conversely, depletion of Med12-Med13 affects the expression of ribosomal protein genes and fibrillarin, indicating a more severe reduction in ribosome biogenesis and cellular growth compared to the loss of CDK8-CycC. Moreover, we found that the stability of CDK8 and CycC relies on Med12 and Med13, with a mutually interdependent relationship between Med12 and Med13. Furthermore, CycC stability depends on the other three CKM subunits. These findings reveal distinct roles for CKM subunits in vivo, with Med12-Med13 disruption exerting a more pronounced impact on ribosome biogenesis and cellular growth compared to the loss of CDK8-CycC. SignificanceThe CDK8 kinase module (CKM), comprising CDK8, CycC, Med12, and Med13, is essential in the Mediator complex for RNA polymerase II-dependent transcription in eukaryotes. While expected to function jointly, CKM subunit mutations result in distinct phenotypes in Drosophila. This study investigates the mechanisms driving these differing effects. Our analysis reveals the role of Med12-Med13 pair in regulating ribosomal biogenesis and cellular growth, contrasting with the involvement of CDK8-CycC in E2F1-dependent cell-cycle progression. Additionally, an asymmetric interdependence in the stability of CDK8-CycC and Med12-Med13 was observed. CKM mutations or overexpression are associated with cancers and cardiovascular diseases. Our findings underscore the distinct impacts of CKM mutations on cellular growth and proliferation, advancing our understanding of their diverse consequences in vivo.

cell biology↗

Nutrient addition in grasslands worldwide reveals proportional plant diversity decline across spatial scales but little change in beta diversity

Nutrient enrichment typically causes local plant diversity declines. A common but untested expectation is that nutrient enrichment also reduces variation in nutrient conditions among localities and selects for a smaller pool of species, causing greater diversity declines at larger than local scales and thus biotic homogenization. Here we apply a framework that links changes in species richness across scales to changes in the numbers of spatially restricted and widespread species for a standardized nutrient addition experiment across 72 grasslands on six continents. Overall, we find proportionally similar species loss at local and larger scales, suggesting similar declines of spatially restricted and widespread species, and no biotic homogenization after 4 years and up to 14 years of treatment. These patterns of diversity changes are generally consistent across species groups. Thus, nutrient enrichment poses threats to plant diversity, including for widespread species that are often critical for ecosystem functions.

ecology↗

Impaired central pattern generators due to abnormal EPHA4 signaling leads to idiopathic scoliosis

Idiopathic scoliosis (IS) is the most common form of spinal deformity with unclear pathogenesis. In this study, we firstly reanalyzed the loci associated with IS, drawing upon previous studies. Subsequently, we mapped these loci to candidate genes using either location-based or function-based strategies. To further substantiate our findings, we verified the enrichment of variants within these candidate genes across several large IS cohorts encompassing Chinese, East Asian, and European populations. Consequently, we identified variants in the EPHA4 gene as compelling candidates for IS. To confirm their pathogenicity, we generated zebrafish mutants of epha4a. Remarkably, the zebrafish epha4a mutants exhibited pronounced scoliosis during later stages of development, effectively recapitulating the IS phenotype. We observed that the epha4a mutants displayed defects in left-right coordination during locomotion, which arose from disorganized neural activation in these mutants. Our subsequent experiments indicated that the disruption of the central pattern generator (CPG) network, characterized by abnormal axon guidance of spinal cord interneurons, contributed to the disorganization observed in the mutants. Moreover, when knocked down efnb3b, the ligand for Epha4a, we observed similar CPG defects and disrupted left-right locomotion. These findings strongly suggested that ephrin B3-Epha4 signaling is vital for the proper functioning of CPGs, and defects in this pathway could lead to scoliosis in zebrafish. Furthermore, we identified two cases of IS in NGEF, a downstream molecule in the EPHA4 pathway. Collectively, our data provide compelling evidence that neural patterning impairments and disruptions in CPGs may underlie the pathogenesis of IS.

genetics↗

Neurobiological Changes Across Pregnancy: A Longitudinal Investigation

Pregnancy is a period of profound biological transformation. However, we know remarkably little about pregnancy-related brain changes. To address this gap, we chart longitudinal changes in brain structure during pregnancy and explore potential mechanisms driving these changes. Ten participants (Mean age = 28.97 years) are assessed 1-6 times (median = 3) during their pregnancy. Each visit includes anatomical and diffusion-weighted MRI, and assessments of waking salivary hormones, hair hormones, and inflammatory cytokines. Here we observe a reduction in gray matter volume gestational week, while neurite density index (NDI), a proxy of axon density, in white matter tracts increase across pregnancy. Progesterone levels are associated with reductions in brain volumetric measurements, and both progesterone and estradiol levels are linked to increases in NDI in white matter tracts. This study highlights the profound neurobiological changes experienced by pregnant individuals and provides insights into neuroplasticity in adulthood.

neuroscience↗