Biology subjects

Campbell, S.

Publications and source records attributed to Campbell, S..

17 recordsLinked to original sources

bioRxiv2026

Hearts may grow concentrically to balance ATP supply and demand and eccentrically to stabilize titin-based stress

Hearts change their wall thickness (concentric growth) and chamber size (eccentric growth) as they adapt to circulatory demands and the intrinsic function of their contractile cells. Factors associated with wall thickening include variants of sarcomeric proteins that enhance contractility, mitochondrial dysfunction, and hypertension. Chambers can dilate due to many factors including sarcomeric variants that depress contractility and aortic and / or mitral valve insufficiency. Despite intensive study, the mechanisms that regulate cardiac growth remain unclear. It is also uncertain whether inherited variants induce growth via the same mechanisms as more common clinical pathologies, such as hypertension. Here we show that computer simulations of a beating left ventricle reproduce both variant and non-variant-related growth patterns when myocytes grow concentrically to regulate intracellular ATP concentration and eccentrically to maintain titin-based intracellular stress. The simulations support the hypothesis that cardiac growth reflects homeostatic feedback through three interacting systems whereby myocytes add or remove mitochondria and sarcomeres (1) in parallel to match ATP generation to myocardial energy demand, and (2) in series to regulate passive tension, while (3) the autonomic nervous system regulates cardiac power, and thus myocardial ATPase, via baroreflex control. The new framework provides a mechanistic basis for the patterns of eccentric and concentric growth induced by a wide range of clinically-relevant conditions and could facilitate in silico testing of potential therapies for cardiac disease. Significance statementHearts grow in response to both physiological and pathological stimuli. The patterns of concentric (wall thickening / thinning) and eccentric (chamber dilation / constriction) induced by different challenges are well recognized but the underlying mechanisms remain unclear. This work presents simulations of a beating left ventricle where (1) concentric growth is regulated by myocytes attempting to stabilize the intracellular ATP concentration and (2) eccentric growth is regulated by titin-mediated stress. The calculations reproduce the growth associated with inherited variants of sarcomeric proteins, mitochondrial dysfunction, hypertension, and both mitral and aortic valve insufficiency. The new ability to predict cardiac growth and its potential modification by treatments, including myotropes, brings the field closer to in silico optimization of therapy for cardiovascular disease.

biophysics↗

bioRxiv2026

Growth and molecular responses of potato to lunar regolith simulants

BackgroundOn-site food production will be required to achieve NASAs goal of a sustainable Lunar habitat. Toward this end, the use of fine, soil-like material on the Lunar surface, known as regolith, has been proposed as a plant growth substrate. However, how this substrate may affect plant growth is not well understood. Lunar regolith is devoid of the organic materials that make soils on earth fertile for plant growth, and has been weathered by solar winds, cosmic rays, and micrometeorite impacts. Additionally, regolith at certain lunar sites may contain heavy metals. These metal ions may leech, thus posing challenges with accumulation in plant material. To address and verify the efficacy of regolith-based crop production, we used lunar regolith simulants (LRS). We investigated the effects of LRS on potato (Solanum tuberosum cv Modoc) plant and tuber development, gene expression, and nutrition profiles. ResultsGrowth in LRS negatively impacted the potato plant size and tuber yield. While the degree of impact differed between simulants, all plants grown in LRS were statistically significantly shorter in height than plants grown in control soil. Further experiments with the lunar mare simulant 1E (LMS-1E) show that these effects can be ameliorated through the addition of vermicompost, an organic component, with a 70:30 v/v ratio of LMS-1E to compost being virtually indistinguishable from controls. Changes in gene expression profiles also differed between simulants, with genes related to photosynthesis, biotic and abiotic stress responses, signaling, and terpenes and flavonoids metabolism being commonly altered. Despite these observed differences in transcription, broad changes in metabolite profiles were not observed. ConclusionsLRS are clearly stressful on plants. However, amendment of the substrate with composted materials appears to be a viable strategy to alleviate stress. Given these observations, regolith-based agriculture may not be viable for very early food production when organic matter content is low. However, this would improve over time with continual incorporation of organic matter to regolith. As such, we believe regolith-based agriculture is a viable long-term strategy.

plant biology↗

bioRxiv2026

Negative regulation of TH17-mediated inflammation by the nuclear receptor REV-ERBβ

TH17 cells play a central role in several human autoimmune diseases. We and others reported the nuclear receptor, REV-ERB, as a cell-intrinsic repressor of TH17-mediated pathogenicity. REV-ERB{beta}, REV-ERBs closely related family member, is thought to be functionally redundant to REV-ERB, which we sought to explore in TH17-mediated immunity. Our data indicate that deletion of REV-ERB{beta} enhances TH17-mediated pro-inflammatory cytokine expression and exacerbated disease in mouse models of multiple sclerosis and colitis. RNA-sequencing indicates REV-ERB{beta} and REV-ERB do not have similar transcriptional profiles. REV-ERB{beta} does not appear to regulate gene expression through interaction with the classic co-repressor NCoR1, which is in contrast to REV-ERB in TH17 cells, nor does it utilize heme, its known endogenous ligand for its repressive functions. Our results establish that while REV-ERB{beta} also acts as a negative regulator of TH17-cell function and pathogenicity, it does so in a manner that is non-redundant, independent, and unique to REV-ERB.

immunology↗

bioRxiv2026

ThermiQuantTM AquaStream: A Portable Instrument for Quantitative Colorimetric Isothermal Nucleic Acid Amplification Reactions in Paper and Tube Formats

Microfluidic paper-based analytical devices ({micro}PADs) are an attractive format for colorimetric nucleic acid amplification tests (NAATs) because they enable low-cost, portable diagnostics in resource-limited settings. However, researchers often optimize colorimetric assays in liquid reactions in tubes before translating them to {micro}PADs. Since both formats require separate instruments for incubation and real-time sensing, direct comparison of reactions between the two formats is difficult. To address these cross-platform limitations, we developed ThermiQuant AquaStream, a portable benchtop device (15 x 20 x 16 cm, [~]5 kg; cost: USD 327) that supports seamless colorimetric loop-mediated isothermal amplification (LAMP) reactions in both {micro}PADs and tubes under a common workflow. The system enables real-time reaction tracking (every 30 seconds) through onboard image processing, precise isothermal control ({+/-}0.5 {degrees}C) using a repurposed consumer-grade sous-vide heater, and medium-throughput (24 tubes or 42 {micro}PADs). Testing with synthetic SARS-CoV-2 orf7ab DNA fragments demonstrated a limit of detection corresponding to a 95% probability of detection (LOD95) of 110 copies per reaction in tube (22 copies/{micro}L) and 39 copies per reaction in {micro}PADs (5 copies/{micro}L), estimated using probit regression. In both formats the limit of quantification (LOQ), defined as the lowest concentration yielding a coefficient of variation (CV) of Tq [≤] 10%, was 250 copies/reaction resulting in a strong linear (R2 = 0.98 & R2 = 0.96 respectively for tube and {micro}PADs) standard calibration curves. ThermiQuant AquaStream provides an affordable and versatile benchtop platform capable of supporting both tube- and {micro}PAD-based colorimetric LAMP assays, serving as a proof-of-concept research tool for assay development and molecular diagnostics in One Health settings such as clinics, farms, and field environments.

bioengineering↗

bioRxiv2025

Pantetheinamides that inhibit the growth of intracellular Salmonella Typhimurium

The metabolic adaptability of intracellular pathogens, such as the Gram-negative Salmonella enterica serovar Typhimurium (STm), enables their survival in nutrient-restricted host environments, while also presenting an opportunity for selective antimicrobial targeting. Herein, we report the synthesis and screening of a small pantetheinamide library aimed at inhibiting the proliferation of STm within macrophages. Two lead compounds exhibited selective activity against intracellular STm and reduced bacterial burden in a murine colitis model. Mechanistic studies suggest their primary mode of action to be the inhibition of coenzyme A (CoA) biosynthesis via the PanD-PanZ regulatory complex, which is absent in host cells. Importantly, resistance pressure to our compound was shown to be significantly stronger in nutrient-limited media compared to nutrient-rich media, supporting the targeting of nutrient stress as a strategy to delay resistance. This work highlights the value of inhibiting pathogen-specific metabolic vulnerabilities in combination with host defence mechanisms to develop novel antimicrobials.

microbiology↗

bioRxiv2025

ARF6 controls VSMC cell phenotypic switching upon lipid stimulation to promote inflammatory signaling contributing to the progression of atherosclerosis

Vascular smooth muscle cells (VSMCs) play a pivotal role in the development and progression of atherosclerosis. Traditionally viewed as contractile cells that maintain vascular tone and structure, VSMCs undergo phenotypic switching in response to atherogenic stimuli, such as high circulating levels of LDL, thus adopting synthetic, osteogenic, or macrophage-like phenotypes. This plasticity contributes to plaque formation, extracellular matrix remodeling, and inflammatory signaling. We have previously shown that ADP-ribosylation factor 1 (ARF1), a small GTP-binding protein, regulates the expression and function of actin, which is important for maintaining the contractile phenotype of VSMCs. However, the role of ARF6 in phenotypic switching remains to be elucidated. Here, we demonstrate that ARF6 knockdown in human aortic smooth muscle cells (HASMCs) reduced lipid uptake through alterations in the expression of scavenger receptors (LOX-1, MSR1), cytokine production (IL-6) as well as modulation of inflammatory markers and pathways (adhesion molecules, PI3K, NFkB, p38). To confirm our findings in an in vivo setting, we engineered a novel conditional smooth muscle cell-specific ARF6 KO mouse in an atheroprone background (Acta2-Cre-ERT2+/-/ApoE-/-/Arf6f/f mice). Mice were fed a high-fat diet to accelerate plaque formation. ARF6 knockout resulted in a significant reduction of atherosclerotic lesions in the aortic arch, which was associated with a reduction of collagen and foam cells. Furthermore, we observed that ARF6 regulates the expression of inflammatory markers. These findings highlight the importance of ARF6 expression in VSMCs and its role in the pathogenesis of atherosclerosis.

biochemistry↗

bioRxiv2025

Genetic background sets the trajectory of cancer evolution

Human cancers are heterogeneous. Their genomes evolve from genetically diverse germlines in complex and dynamic environments, including exposure to potential carcinogens. This heterogeneity of humans, our environmental exposures, and subsequent tumours makes it challenging to understand the extent to which cancer evolution is predictable. Addressing this limitation, we re-ran early tumour evolution hundreds of times in diverse, inbred mouse strains, capturing genetic variation comparable to and beyond that found in human populations. The sex, environment, and carcinogenic exposures were all controlled and tumours comprehensively profiled with whole genome and transcriptome sequencing. Within a strain, there was a high degree of consistency in the mutational landscape, a limited range of driver mutations, and all strains converged on the acquisition of a MAPK activating mutation with similar transcriptional disruption of that pathway. Despite these similarities in the phenotypic state of tumours, different strains took markedly divergent paths to reach that state. This included pronounced biases in the precise driver mutations, the strain specific occurrence of whole genome duplication, and differences in subclonal selection that reflected both cancer susceptibility and tumour growth rate. These results show that interactions between the germline genome and the environment are highly deterministic for the trajectory of tumour genome evolution, and even modest genetic divergence can substantially alter selection pressures during cancer development, influencing both cancer risk and the biology of the tumour that develops.

genomics↗

bioRxiv2024

Functional and evolutionary constraints of wtf killer meiotic drivers

Killer meiotic drivers are selfish DNA loci that sabotage the gametes that do not inherit them from a driver+/driver- heterozygote. These drivers often employ toxic proteins that target essential cellular functions to cause the destruction of driver- gametes. Identifying the mechanisms of drivers can expand our understanding of infertility and reveal novel insights about the cellular functions targeted by drivers. In this work, we explore the molecular mechanisms underlying the wtf family of killer meiotic drivers found in fission yeasts. Each wtf killer acts using a toxic Wtfpoison protein that can be neutralized by a corresponding Wtfantidote protein. The wtf genes are rapidly evolving and extremely diverse. Here we found that self-assembly of Wtfpoison proteins is broadly conserved and associated with toxicity across the gene family, despite minimal amino acid conservation. In addition, we found the toxicity of Wtfpoison assemblies can be modulated by protein tags designed to increase or decrease the extent of the Wtfpoison assembly, implicating assembly size in toxicity. We also identified a conserved, critical role for the specific co-assembly of the Wtfpoison and Wtfantidote proteins in promoting effective neutralization of Wtfpoison toxicity. Finally, we engineered wtf alleles that encode toxic Wtfpoison proteins that are not effectively neutralized by their corresponding Wtfantidote proteins. The possibility of such self-destructive alleles reveals functional constraints on wtf evolution and suggests similar alleles could be cryptic contributors to infertility in fission yeast populations. As rapidly evolving killer meiotic drivers are widespread in eukaryotes, analogous self-killing drive alleles could contribute to sporadic infertility in many lineages. Author SummaryDiploid organisms, such as humans, have two copies of most genes. Only one copy, however, is transmitted through gametes (e.g., sperm and egg) to any given offspring. Alternate copies of the same gene are expected to be equally represented in the gametes, resulting in random transmission to the next generation. However, some genes can "cheat" to be transmitted to more than half of the gametes, often at a cost to the host organism. Killer meiotic drivers are one such class of cheater genes that act by eliminating gametes lacking the driver. In this work, we studied the wtf family of killer meiotic drivers found in fission yeasts. Each wtf driver encodes a poison and an antidote protein to specifically kill gametes that do not inherit the driver. Through analyzing a large suite of diverse natural and engineered mutant wtf genes, we identified multiple properties--such as poison self-assembly and poison-antidote co-assembly--that can constrain poison toxicity and antidote rescue. These constraints could influence the evolution of wtf genes. Additionally, we discovered several incompatible wtf poison-antidote pairs, demonstrating expanded potential for self-killing wtf alleles. Such alleles could potentially arise spontaneously in populations cause infertility.

genetics↗

bioRxiv2023

Noisy delay denoises biochemical oscillators

Genetic oscillations are generated by delayed transcriptional negative feedback loops, wherein repressor proteins inhibit their own synthesis after a temporal production delay. This delay is distributed because it arises from a sequence of noisy processes, including transcription, translation, folding, and translocation. Because the delay determines repression timing and therefore oscillation period, it has been commonly believed that delay noise weakens oscillatory dynamics. Here, we demonstrate that noisy delay can surprisingly denoise genetic oscillators. Moderate delay noise unexpectedly sharpens oscillation peaks and improves temporal peak reliability without impacting period. We show that this denoising phenomenon occurs in a variety of well-studied genetic oscillators and we use queueing theory to uncover the universal mechanisms that produce it.

systems biology↗

bioRxiv2021

Extinction risk modeling predicts range-wide differences of climate change impact on Karner blue butterfly

Withdrawal StatementThe authors have withdrawn their manuscript owing to the fact that the manuscript has not gone through the US Geological Survey review and approval process required prior to posting and is, therefore, withdrawn. Therefore, the authors do not wish this work to be cited as reference for the project. If you have any questions, please contact the corresponding author.

ecology↗

bioRxiv2021

Computational model of 3D cell migration based on the molecular clutch mechanism

The external environment is a regulator of cell activity. Its stiffness and microstructure can either facilitate or prevent 3D cell migration in both physiology and disease. 3D cell migration results from force feedbacks between the cell and the extracellular matrix (ECM). Adhesions regulate these force feedbacks by working as molecular clutches that dynamically bind and unbind the ECM. Because of the interdependency between ECM properties, adhesion dynamics, and cell contractility, how exactly 3D cell migration occurs in different environments is not fully understood. In order to elucidate the effect of ECM on 3D cell migration through force-sensitive molecular clutches, we developed a computational model based on a lattice point approach. Results from the model show that increases in ECM pore size reduce cell migration speed. In contrast, matrix porosity increases it, given a sufficient number of ligands for cell adhesions and limited crowding of the matrix from cell replication. Importantly, these effects are maintained across a range of ECM stiffnesses, demonstrating that mechanical factors are not responsible for how matrix microstructure regulates cell motility.

biophysics↗

bioRxiv2020

kTWAS: integrating kernel-machine with transcriptome-wide association studies improves statistical power and reveals novel genes

The power of genotype-phenotype association mapping studies increases greatly when contributions from multiple variants in a focal region are meaningfully aggregated. Currently, there are two popular categories of variant aggregation methods. Transcriptome-wide association studies (TWAS) represent a category of emerging methods that select variants based on their effect on gene expressions, providing pretrained linear combinations of variants for downstream association mapping. In contrast, kernel methods such as SKAT model genotypic and phenotypic variance using various kernel functions that capture genetic similarity between subjects, allowing non-linear effects to be included. From the perspective of machine learning, these two methods cover two complementary aspects of feature engineering: feature selection/pruning, and feature modeling. Thus far, no thorough comparison has been made between these categories, and no methods exist which incorporate the advantages of TWAS and kernel-based methods. In this work we developed a novel method called kTWAS that applies TWAS-like feature selection to a SKAT-like kernel association test, combining the strengths of both approaches. Through extensive simulations, we demonstrate that kTWAS has higher power than TWAS and multiple SKAT-based protocols, and we identify novel disease-associated genes in WTCCC genotyping array data and MSSNG (Autism) sequence data. The source code for kTWAS and our simulations are available in our GitHub repository (https://github.com/theLongLab/kTWAS).

bioinformatics↗

bioRxiv2019

Distinctive epigenomic alterations in NF1-deficient cutaneous and plexiform neurofibromas drive differential MKK/P38 signaling

Benign peripheral nerve sheath tumors are the clinical hallmark of Neurofibromatosis Type 1. They account for substantial morbidity in NF1 and are difficult to manage. Cutaneous (CNF) and plexiform neurofibromas (PNF) share identical histology, but maintain different growth rates and risk of malignant conversion. The reasons for their disparate clinical behavior are not well explained on the basis of recent genome or transcriptome profiling studies. We hypothesized that CNFs and PNFs are epigenetically distinct tumor types that exhibit differential signaling due to genome-wide and site-specific methylation events. We interrogated the methylation profiles of 45 CNFs and 17 PNFs (Illumina EPIC 850K) using normal tissue controls from NF1 subjects. Based on these profiles, we confirm that CNFs and PNFs are epigenetically distinct tumors with broad differences in higher order chromatin states, and specific methylation events altering genes involved in key biological and cellular processes such as inflammatory mediator regulation of TRP channels, RAS/MAPK signaling, actin cytoskeleton rearrangement, and oxytocin signaling. Based our identification of 2 separate DMRs associated with alternative leading exons in MAP2K3, we demonstrate differential RAS/MKK3/P38 signaling between CNFs and PNFs. Epigenetic reinforcement of RAS/MKK/P38 was a defining characteristic of CNFs leading to pro-inflammatory signaling and chromatin conformational changes, whereas PNFs signaled predominantly through RAS/ERK. Tumor size also correlated with specific CpG methylation events. Taken together, these findings confirm that epigenetic regulation of RAS signaling fates accounts for observed differences in CNF and PNF clinical behavior. CNFs may also respond differently than PNFs to RAS-targeted therapeutics raising the possibility of targeting P38-mediated inflammation for CNF treatment.

genomics↗

bioRxiv2019

Computational model demonstrates that Ndc80-associated proteins strengthen kinetochore-microtubule attachments in metaphase

Chromosome segregation is mediated by spindle microtubules that attach to kinetochore via dynamic protein complexes, such as Ndc80, Ska, Cdt1 and ch-TOG during mitotic metaphase. While experimental studies have previously shown that these proteins and protein complexes are all essential for maintaining a stable kinetochore-microtubule interface, their exact roles in this process remains elusive. In this study, we employed experimental and computational methods in order to characterize how these proteins can strengthen kMT attachments in both non load-bearing and load-bearing conditions, typical of prometaphase and metaphase, respectively. Immunofluorescence staining of Hela cells showed that the levels of Ska and Cdt1 significantly increase from prometaphase to metaphase. Our new computational model showed that, by incorporating binding and unbinding of each protein complex, coupled with a biased diffusion mechanism, the displacement of a possible complex formed by Ndc80-Ska-Cdt1 is significantly higher than that formed by Ndc80 alone or Ndc80-Ska. In addition, when we use Ndc80/ch-TOG in the model, rupture force and time of attachment of the kMT interface increases. These results support the hypothesis that Ndc80-associated proteins strengthen kMT attachments and that it is the interplay between kMT protein complexes in metaphase that ensures stable attachments.

cell biology↗

bioRxiv2019

A microwell cell capture device reveals variable response to dobutamine in isolated cardiomyocytes

Isolated ventricular cardiomyocytes exhibit substantial cell-to-cell variability, even when obtained from the same small volume of myocardium. In this study, we investigated the possibility that cardiomyocyte responses to {beta}-adrenergic stimulus are also highly heterogeneous. In order to achieve the throughput and measurement duration desired for these experiments, we designed and validated a novel microwell system that immobilizes and uniformly orients isolated adult cardiomyocytes. In this configuration, detailed drug responses of dozens of cells can be followed in parallel for intervals exceeding one hour. At the conclusion of an experiment, specific cells can also be harvested via a precision aspirator for single-cell gene expression profiling. Using this system, we followed changes in Ca2+ signaling and contractility of individual cells under sustained application of either dobutamine or omecamtiv mecarbil. Both compounds increased average cardiomyocyte contractility over the course of an hour, but responses of individual cells to dobutamine were significantly more variable. Surprisingly, some dobutamine-treated cardiomyocytes augmented Ca2+ release without increasing contractility. Other cells responded with increased contractility in spite of unchanged Ca2+ release. Single-cell gene expression analysis revealed a significant correlation between expression of PRKACA and cellular sensitivity to dobutamine, demonstrating that variable drug responses among cells are not merely experimental artifacts. By enabling direct comparison of the functional behavior of an individual cell and the genes it expresses, this new system constitutes a unique tool for interrogating cardiomyocyte drug responses and discovering the genes that modulate them.\n\nSIGNIFICANCEWe have created a microwell capture device that allows drug responses of dozens of isolated adult cardiomyocytes to be monitored for extended intervals. Using the device, we observed striking diversity in the Ca2+ handling and contractility responses of each cell to a {beta}-adrenergic agonist. This included cells that responded to dobutamine by doubling the amplitude of Ca2+ release while decreasing contractility and vice-versa. We further show that these diverse responses can be linked to gene expression differences between cells. This work demonstrates the feasibility of linking the drug responses of individual cells with their gene expression. It opens the possibility of exploiting cell-to-cell variation to discover new genes that participate in and modulate regulatory cascades.

physiology↗

bioRxiv2019

Insight into the genetic aetiology of retinal detachment by combining small clinical and large population-based datasets

Idiopathic retinal detachment is a serious common condition, but genetic studies to date have been hampered by the small size of the assembled cohorts. Genetic correlations between retinal detachment and high myopia or cataract operation were high, respectively 0.46 (SE=0.08) and 0.44 (SE=0.07), in the UK Biobank dataset and in line with known epidemiological associations. Meta-analysis of genome-wide association studies using UK Biobank retinal detachment cases (N=3977) and two cohorts, each comprising [~]1000 rhegmatogenous retinal detachment patients, uncovered 11 genome-wide significant association signals, near or within ZC3H11B, BMP3, COL22A1, DLG5, PLCE1, EFEMP2, TYR, FAT3, TRIM29, COL2A1 and LOXL1. Replication in the 23andMe dataset, where retinal detachment is self-reported by participants, firmly establishes association at six loci FAT3, COL22A1, TYR, BMP3, ZC3H11B and PLCE1. The former two seem to particularly impact on retinal detachment, the latter three shed light on shared aetiologies with cataract, myopia and glaucoma.\n\nAuthor SummaryRetinal detachments are common conditions that may lead to permanent severe sight reduction or blindness; they are a major cause of emergency eye surgery. The most common type of retinal detachment follows a break in the retina and is thought to be in part genetically determined but little is known about the contributing individual genetic risk variants. The condition prevalence increases with age and with common eye conditions such as myopia, cataract or glaucoma. We showed that the retinal detachment cases derived from self-report or hospitalisation records in the large UK Biobank dataset show very similar characteristics to samples of carefully clinically evaluated retinal detachment with break cases and therefore could be used to perform genetic analysis of the condition. Association studies require large sample of cases and by pooling Biobank and clinical cases, this study identifies 11 novel significant associations, six of which were further replicated in an independent population-based dataset (23andMe). Two of the replicated findings seem to specifically underline retinal detachment risk while three others highlight shared genetic risk with myopia, cataract and/or glaucoma, paving the way to better understanding of these conditions and of their overlap.

genetics↗

bioRxiv2017

2D:4D and spatial abilities: From rats to humans

Variance in spatial abilities are thought to be determined by in utero levels of testosterone and oestrogen, measurable in adults by the length ratio of the 2nd and 4th digit (2D:4D). We confirmed the relationship between 2D:4D and spatial performance using rats in two different tasks (paired-associate task and watermaze) and replicated this in humans. We further clarified anatomical and functional brain correlates of the association between 2D:4D and spatial performance in humans.

neuroscience↗