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Taylor, P.

Publications and source records attributed to Taylor, P..

At least 19 recordsLinked to original sources

Agency and Embodiment Provide Dissociable Benefits to Perception, Metacognition and Neural Processing During Active Sensing

Metacognition, judging how reliable our own perceptual decisions are, is central to adaptive behavior. Such judgments hinge on the reliability of the sensory evidence on which that decision is based, and active sensing through self-directed exploration is known to improve perception itself. Yet, how agency, the authorship over self-initiated actions, and the processing of the sensory consequences, which is implicit to active sensing, modulate metacognition and its calibration, remains unknown. Whether physical embodiment adds to this beyond virtual exploration is similarly unclear, yet relevant both for daily life and for self-monitoring in agentic AI. Here, we combined a naturalistic auditory search paradigm with mobile electroencephalography. Twenty participants performed a target-detection task under three conditions: active embodied exploration , active screen-based exploration, and passive listening to replays of their own trials, while we obtained steady-state auditory evoked potentials (SSAEPs) to characterize stimulus-locked neural responses. We find that both agency conditions improved accuracy, metacognitive sensitivity, and overall SSAEP amplitude relative to passive listening, indicating that agency, rather than whole-body movement, drives these enhancements. Crucially, however, embodiment uniquely grounded both the target-evoked neural response and the subjects' confidence to immediate sensory evidence. Thus, agency alone broadly enhances perceptual and neural processing, but embodiment specifically anchors confidence, neurally and behaviorally, to the present.

neuroscience↗

Traveling brain waves support flexible storage of human working memory

Human working memory enables us to temporarily store and flexibly utilize information. It is thought that there are two distinct neural mechanisms by which information is retained in working memory: persistent firing of working memory-relevant neurons, or short-term synaptic plasticity in the absence of ongoing neuronal firing. However, both these mechanisms can lead to strong neural interference when working memory contents are updated with novel information. As an alternative, here we propose that information can be flexibly held in working memory in the form of traveling waves - spatiotemporal patterns of neural activity that propagate across brain tissue. In an artificial neural network, we simulated wave propagation by passing transient neural firing patterns representative of single-item information across different network layers. In comparison to sustained neural firing, we demonstrate that these transient traveling waves result in minimal synaptic plasticity, thereby facilitating working memory updating without significant neural interference. We then identified such traveling waves in intracranial recordings from the human temporal lobe. Traveling waves started precisely when information was being encoded and persisted uniformly throughout maintenance and recall, aligning with the activation pattern seen in the artificial neural network. In trials where participants committed memory errors, no such continuous traveling wave activity in the temporal lobe was observed. Our data from artificial neural networks and human intracranial brain recordings converge to indicate that neural traveling waves support information processing in working memory while minimizing interference during updating. This reported mechanism, together with the classical working memory models, serves as a mutually complementary, multi-mechanistic framework for working memory storage.

neuroscience↗

Atypical BlaIR Two-Component System in Pseudomonas aeruginosa Regulates Virulence but not β-Lactam Resistance

With the rise of antimicrobial resistance, anti-virulence therapeutics are a viable alternative to circumvent resistance pressures. Hypothetical genes and proteins are an under-studied source of potential virulence factor targets. We performed bioinformatic analyses to identify conserved hypothetical genes enriched in pathogenic Pseudomonas aeruginosa but not in non-pathogenic strains. This analysis identified an atypical BlaIR system, which we named pvmSR, that regulated P. aeruginosa virulence in a Caenorhabditis elegans infection model. This is in contrast with the typical BlaIR system from Staphylococcus aureus, which regulates resistance to {beta}-lac-tam antibiotics. The{Delta} pvmSR mutant showed reduced virulence in a C. elegans slow-killing assay. To understand how PvmSR regulated virulence in vivo, we performed dual RNA-seq to analyze transcriptomic changes in both C. elegans and P. aeruginosa. We found that C. elegans responded to P. aeruginosa {Delta}pvmSR infection by decreasing expression of lysosome and phagocytosis pathways. In P. aeruginosa {Delta}pvmSR, we observed decreased gene expression of several known virulence factors including the hydrogen cyanide synthase, hcnC, and heparinase, hepP. Additionally, we observed dysregulation in genes important for quorum sensing and biofilm formation. Collectively, our findings indicated that PvmSR contributed to virulence regulation and may serve as a potential anti-virulence target.

microbiology↗

Decoding real world visual scenes from the human gamma band with flicker evoked oscillations.

Current approaches to investigate the role of neural oscillations in natural scene processing have been limited to artificial stimuli and long data collection. We present a new way to decode real-world scenes participants are viewing from the steady-state visual evoked potentials (SSVEPs) evoked while wearing flickering LCD glasses. We discovered that SSVEP responses from real world scenes are surprisingly complex and have distinct waveform shapes: they differ markedly across scenes and participants but are consistent within individuals, even across multiple days. SSVEP shape varies greatly between stimuli, but is reliable, meaning that decoding works even with a single electrode. Decoding is highly accurate with 5-10 seconds of data and was still above chance level with less than a second of data. Decomposing the SSVEPs into frequency bands showed that the information about the visual scene is present across all of the harmonics of the flicker frequency, but with 40 Hz (gamma band) showing the highest amount of information across the different flicker frequencies tested. These findings implicate a broad range of oscillations in encoding real-world scenes, with a particular importance for 40 Hz. The SSVEPs temporal profile is a rich source of information for decoding.

neuroscience↗

Contralateral Prefrontal and Network Engagement during Left DLPFC 10 Hz rTMS: An Interleaved TMS-fMRI Study in Healthy Adults

BackgroundHigh-frequency repetitive transcranial magnetic stimulation (rTMS) over the left dorsolateral prefrontal cortex (DLPFC) serves as an effective treatment for major depression and other psychiatric disorders. Despite its growing clinical application, the neural mechanisms by which prefrontal rTMS exerts its therapeutic effects remain incompletely understood. To address this gap, we investigated the immediate blood-oxygen-level-dependent (BOLD) activity during 600 stimuli of left DLPFC 10 Hz rTMS in healthy individuals using interleaved TMS-fMRI. MethodsIn a crossover design, 17 healthy subjects received 10 Hz rTMS (60 trains with 9-second intertrain intervals) over the left DLPFC at 40% and 80% of their resting motor threshold (rMT) inside the MR scanner. Results10 Hz rTMS over the left DLPFC elicited BOLD responses in prefrontal regions, cingulate cortex, insula, striatum, thalamus, as well as auditory and somatosensory areas. Notably, our findings revealed that 10 Hz rTMS effects were lateralized towards the contralateral (right) DLPFC. Dose-response effects (40% vs. 80% rTMS) were exclusively observed in contralateral subcortical regions, whereas dose-responses within the DLPFC showed substantial inter-individual variability. ConclusionsThe 10 Hz rTMS protocol used in this study induced distinct target engagement and propagation patterns in the prefrontal cortex. These patterns differ from our previous interleaved TMS-fMRI findings using 600 stimuli of left DLPFC intermittent theta burst stimulation (iTBS) at the same intensities. Thus, interleaved TMS-fMRI emerges as a valuable method for comparing clinical prefrontal rTMS protocols regarding their immediate effect on brain circuits in order to differentiate their action mechanisms and to potentially inform clinical applications.

neuroscience↗

Visually Evoked 40 Hz Gamma Activity Enhanced by Transcranial Electrical Stimulation

ObjectiveTranscranial Electrical Stimulation and Visual Stimulation in the gamma band (30-100 Hz, especially 40 Hz) are increasingly used to study and even enhance human cognition. Combining both techniques would be of scientific and clinical value, provided that Steady-State Visually Evoked Potentials (SSVEPs) are measured concurrently to determine any neuronal effects of the electrical brain stimulation. This poses a substantial methodological challenge. We aimed to demonstrate that recording visually evoked 40 Hz activity with EEG during electrical brain stimulation is possible and to explore potential interactions. ApproachWe tested if electrical and visual stimulation might interact depending on which brain areas are electrically stimulated (Experiment 1; N=25) and how closely the respective frequencies match (Experiment 2; N=25). Experiment 3 (N=25) assessed how effectively the data processing pipeline can mitigate electrical artefacts and recover real evoked neuronal activity. SSVEPs were processed and analysed in the time domain using an optimised adaptive template subtraction approach. Main Results40 Hz SSVEPs were successfully recorded during frequency-matched electrical stimulation applied between central and occipital regions. Waveform correlations revealed that SSVEPs from combined visual and electrical stimulation were more similar in shape to baseline SSVEPs from visual stimulation alone than to control data from electrical stimulation alone. Accordingly, during combined stimulation, the recovered signals were stronger in amplitude than the electrical control data. We found no evidence of interactions between electrical and visual stimulation. SignificanceWe demonstrated that 40 Hz SSVEPs can be reliably measured with EEG during frequency-matched electrical brain stimulation, distinguishing neuronal activity from electrical or physiological confounds. This method enables fundamental and clinical researchers to combine rhythmic sensory and electrical stimulation in the gamma band and concurrently quantify neuronal electrophysiological effects.

neuroscience↗

A first insight into the developability of an IgG3: A combined computational and experimental approach

Immunoglobulin G 3 (IgG3) monoclonal antibodies (mAbs) are high value scaffolds for developing novel therapies. Despite their wide-ranging therapeutic potential, IgG3 physicochemical properties and developability characteristics remain largely under-characterised. Protein-protein interactions elevate solution viscosity in high-concentration formulations impacting physico-chemical stability, manufacturability, and injectability of mAbs. Therefore, in this manuscript, the key molecular descriptors and biophysical properties of a model anti-IL-8 IgG1 and its IgG3 ortholog are characterised. A computational and experimental framework was applied to measure molecular descriptors impacting on their downstream developability. Findings from this approach underpin a detailed understanding of the molecular characteristics of IgG3 mAbs as potential therapeutic entities. This work is the first report examining the manufacturability of IgG3 for high concentration mAb formulations. While poorer conformational and colloidal stability, and elevated solution viscosity was observed for IgG3, future efforts controlling surface potential through sequence-engineering of solvent-accessible patches can be used to improve biophysical parameters that dictate mAb developability.

bioengineering↗

Uncoupling of synaptic loss from amyloid burden by an Alzheimer's disease protective variant of PLCγ2.

A rare coding missense variant (rs72824905; P522R) in PLCG2 decreases the risk of late-onset Alzheimers disease, but how this protective effect is mediated is unclear. Here we demonstrate a mechanism for this protection, the R522 variant of PLC{gamma}2 alters microglial activity leading to a marked preservation of synaptic integrity and reduced peri-plaque microglial engulfment of synapses independently of amyloid burden. Our data advocate for a direct central role of PLC{gamma}2 in mediating synaptic loss as part of the pathological process of Alzheimers disease (AD), prioritising it as a therapeutic target and modulator of disease.

neuroscience↗

Sex-specific Proximal Tubular Cell differentiation pathways identified by single-nucleus RNA

BackgroundPostpartum kidney growth is substantial but proliferation and differentiation pathways underpinning nephron elongation are not well defined. Here we performed sequential characterization of mouse kidney transcriptomics at the single cell level to address this. MethodsSingle nuclear RNA sequencing (snRNA-seq) was performed on kidney tissue from male and female mice at 1, 2, 4 and 12 weeks of age using the 10x Chromium platform. ResultsUnbiased clustering was performed on 68,775 nuclei from 16 animals. 31 discrete cellular clusters were seen, which were identified through comparison of their gene expression profiles to canonical markers of kidney cell populations. High levels of proliferation were evident at early time points in some cell types, especially tubular cells, but not in other cell types, for example podocytes. Proliferation was especially evident in Proximal Tubular Cells (PTCs) which are the most abundant cell type in the adult kidney. Uniquely when compared to other kidney cell types, PTCs demonstrated sex-specific expression profiles at late, but not early, time points. Mapping of PTC differentiation pathways using techniques including trajectory and RNA Velocity analyses delineated increasing PTC specialization and sex-specific phenotype specification. ConclusionOur single-cell transcriptomics data characterise cellular states observed during kidney growth. We have identified PTC differentiation pathways that lead to sex-specific tubular cell phenotypes.

cell biology↗

Atopic dermatitis complicated by recurrent eczema herpeticum is characterized by multiple, concurrent epidermal inflammatory endotypes

BACKGROUNDA subgroup of atopic dermatitis (AD) patients suffer from recurrent, disseminated herpes simplex virus (HSV) skin infections, termed eczema herpeticum (EH), which can be life-threatening and contribute to AD morbidity. The pathobiology underlying ADEH is unknown. OBJECTIVETo determine transcriptional mechanisms of skin and immune system pathobiology that underlie ADEH disease. METHODSWe performed whole transcriptome RNA-sequencing of non-lesional skin samples (epidermis, dermis) of AD patients with (ADEH+, n=15) and without (ADEH-, n=13) recurrent EH history, and healthy controls (HC, n=15). We also performed RNA-sequencing on plasmacytoid dendritic cells (pDCs) collected from these participants and infected in vitro with HSV-1. Differential expression, gene set enrichment, and endotyping analyses were performed. RESULTSADEH+ disease was characterized by dysregulation in skin gene expression, which was limited in dermis (differentially expressed genes [DEGs]=14) and widespread in epidermis (DEGs=129). ADEH+-upregulated epidermal DEGs were enriched in type 2 cytokine (T2) (IL4R, CCL22, CRLF2, IL7R), interferon (CXCL10, ICAM1, IFI44, and IRF7), and IL-36{gamma} (IL36G) inflammatory pathway genes. At a person-level, all ADEH+ participants exhibited T2 and interferon endotypes and 87% were IL36G-high. In contrast, these endotypes were more variably expressed among ADEH- participants. ADEH+ patient skin also exhibited dysregulation in epidermal differentiation complex (EDC) genes within the LCE, S100, and SPRR families, which are involved in skin barrier function, inflammation, and antimicrobial activities. pDC transcriptional responses to HSV-1 infection were not altered by ADEH status. CONCLUSIONSADEH+ pathobiology is characterized by a unique, multi-faceted epidermal inflammation that accompanies dysregulation in the expression of EDC genes. Key MessagesO_LIAD patients with a history of recurrent EH exhibit molecular skin pathobiology that is similar in form, but more severe in degree, than in AD patients without this complication. C_LIO_LINon-lesional skin of ADEH+ patients concurrently exhibits excessive type 2 cytokine, interferon, and IL-36{gamma}-driven epidermal inflammation. C_LIO_LIExpression of these inflammatory skin endotypes among ADEH+ patients is associated with dysregulation in expression of epidermal differentiation complex genes involved in barrier function, inflammation, and antimicrobial activity. C_LI Capsule SummaryAD patients with a history of recurrent disseminated HSV-1 skin infections form a unique molecular skin endotype group that concurrently exhibits type 2 cytokine, interferon, and IL-36{gamma}-driven skin inflammation, accompanied by dysregulation in expression of epidermal differentiation complex genes involved in barrier function, inflammation, and antimicrobial activity.

molecular biology↗

Effector Th1 cells alter the transcriptional output of IL-6 in acute resolving inflammation

Cytokines that signal via STAT1 and STAT3 transcription factors instruct decisions affecting tissue homeostasis, anti-microbial host defense, and inflammation-induced tissue injury. To understand the coordination of these activities, we applied RNA-seq, ChIP-seq, and ATAC-seq to identify the transcriptional output of STAT1 and STAT3 in peritoneal tissues during acute resolving inflammation and inflammation primed to drive fibrosis. Bioinformatics focussed on the transcriptional signature of the immuno-modulatory cytokine IL-6 in both settings and examined how pro-fibrotic IFN{gamma}-secreting CD4+ T-cells altered the interpretation of STAT1 and STAT3 cytokine cues. In resolving inflammation, STAT1 and STAT3 cooperated to drive stromal gene expression affecting anti-microbial immunity and tissue homeostasis. The introduction of IFN{gamma}-secreting CD4+ T-cells altered this transcriptional program and channeled STAT1 and STAT3 to a previously latent GAS motif in Alu-like elements. STAT1 and STAT3 binding to this conserved sequence revealed evidence of reciprocal cross-regulation and gene signatures relevant to pathophysiology. Thus, we propose that effector T-cells re-tune the transcriptional output of IL-6 by shaping a regulatory interplay between STAT1 and STAT3 in inflammation.

immunology↗

Age-Associated Insolubility of Parkin in Human Midbrain is Linked to Redox Balance and Sequestration of Reactive Dopamine Metabolites

The mechanisms by which parkin protects the adult human brain from Parkinson disease remain incompletely understood. We hypothesized that parkin cysteines participate in redox reactions, which are reflected in its posttranslational modifications. We found that in human control brain, including the S. nigra, parkin is largely insoluble after age 40 years, which is linked to its oxidation, e.g., at Cys95 and Cys253. In mice, oxidative stress increases posttranslational modifications at parkin cysteines and reduces its solubility. Oxidation of recombinant parkin also promotes insolubility and aggregate formation, but in parallel, lowers hydrogen peroxide (H2O2). This thiol-based redox activity is diminished by parkin point mutants, e.g., p.C431F and p.G328E. Intriguingly, in parkin-deficient human brain H2O2 concentrations are elevated. In prkn-null mice, H2O2 levels are dysregulated under oxidative stress conditions, such as acutely by MPTP-toxin exposure or chronically due to a second genetic hit. In dopamine toxicity studies, wild-type parkin, but not disease-linked mutants, protects human dopaminergic M17 cells, in part through lowering H2O2. Parkin also neutralizes reactive, electrophilic dopamine metabolites via adduct formation, which occurs foremost at primate-specific Cys95. Further, wild-type but not p.C95A-mutant parkin augments melanin formation. In sections of normal, adult human midbrain, parkin specifically co-localizes with neuromelanin pigment, frequently within LAMP-3/CD63+ lysosomes. We conclude that oxidative modifications of parkin cysteines are associated with protective outcomes, which include the reduction of H2O2, conjugation of reactive dopamine metabolites, sequestration of radicals within insoluble aggregates, and increased melanin formation. The loss of these redox effects may augment oxidative stress in dopamine producing neurons of mutant PRKN allele carriers, thereby contributing to neurodegeneration.

neuroscience↗

Optimization and scaling of patient-derived brain organoids uncovers deep phenotypes of disease

Cerebral organoids provide unparalleled access to human brain development in vitro. However, variability induced by current culture methodologies precludes using organoids as robust disease models. To address this, we developed an automated Organoid Culture and Assay (ORCA) system to support longitudinal unbiased phenotyping of organoids at scale across multiple patient lines. We then characterized organoid variability using novel machine learning methods and found that the contribution of donor, clone, and batch is significant and remarkably consistent over gene expression, morphology, and cell-type composition. Next, we performed multi-factorial protocol optimization, producing a directed forebrain protocol compatible with 96-well culture that exhibits low variability while preserving tissue complexity. Finally, we used ORCA to study tuberous sclerosis, a disease with known genetics but poorly representative animal models. For the first time, we report highly reproducible early morphological and molecular signatures of disease in heterozygous TSC+/- forebrain organoids, demonstrating the benefit of a scaled organoid system for phenotype discovery in human disease models.

neuroscience↗

Oxylipin metabolism is controlled by mitochondrial b-oxidation during bacterial inflammation.

Oxylipins are potent biological mediators requiring strict control, but how they are removed en masse during infection and inflammation is unknown. Here we show that lipopolysaccharide (LPS) dynamically enhances oxylipin removal via mitochondrial {beta}-oxidation. Specifically, genetic or pharmacological targeting of carnitine palmitoyl transferase 1 (CPT1), a mitochondrial importer of fatty acids, reveal that many oxylipins are removed by this protein during inflammation in vitro and in vivo. Using stable isotope-tracing lipidomics, we find secretion-reuptake recycling for 12-HETE and its intermediate metabolites. Meanwhile, oxylipin {beta}-oxidation is uncoupled from oxidative phosphorylation, thus not contributing to energy generation. Testing for genetic control checkpoints, transcriptional interrogation of human neonatal sepsis finds upregulation of many genes involved in mitochondrial removal of long-chain fatty acyls, such as ACSL1,3,4, ACADVL, CPT1B, CPT2 and HADHB. Also, ACSL1/Acsl1 upregulation is consistently observed following the treatment of human/murine macrophages with LPS and IFN-{gamma}. Last, dampening oxylipin levels by {beta}-oxidation is suggested to impact on their regulation of leukocyte functions. In summary, we propose mitochondrial {beta}-oxidation as a regulatory metabolic checkpoint for oxylipins during inflammation.

biochemistry↗

A collaborative resource platform for non-human primate neuroimaging

Neuroimaging non-human primates (NHPs) is a growing, yet highly specialized field of neuroscience. Resources that were primarily developed for human neuroimaging often need to be significantly adapted for use with NHPs or other animals, which has led to an abundance of custom, in-house solutions. In recent years, the global NHP neuroimaging community has made significant efforts to transform the field towards more open and collaborative practices. Here we present the PRIMatE Resource Exchange (PRIME-RE), a new collaborative online platform for NHP neuroimaging. PRIME-RE is a dynamic community-driven hub for the exchange of practical knowledge, specialized analytical tools, and open data repositories, specifically related to NHP neuroimaging. PRIME-RE caters to both researchers and developers who are either new to the field, looking to stay abreast of the latest developments, or seeking to collaboratively advance the field.

neuroscience↗

Callosal anisotropy predicts attentional network changes after parietal inhibitory stimulation

Hemispatial neglect is thought to result from disruption of interhemispheric equilibrium. Right hemisphere lesions deactivate the right frontoparietal network and hyperactivate the left via release from interhemispheric inhibition. Support for this theory comes from neuropsychological evidence as well as transcranial magnetic stimulation (TMS) studies in healthy subjects, in whom right posterior parietal cortex (PPC) inhibition causes neglect-like, rightward, visuospatial bias. Concurrent TMS and fMRI after right PPC TMS show task-dependent changes but may fail to identify effects of stimulation in areas not directly activated by the specific task, complicating interpretations. We used resting-state functional connectivity (RSFC) after inhibitory TMS over the right PPC to examine changes in the networks underlying visuospatial attention. In a crossover experiment in healthy individuals, we delivered continuous theta burst TMS to the right PPC and vertex as control condition. We hypothesized that PPC inhibitory stimulation would cause a rightward visuospatial bias, decrease PPC connectivity with frontal areas, and increase PPC connectivity with the attentional network in the left hemisphere. We also expected that individual differences in fractional anisotropy (FA) in white matter connections between the PPCs would account for variability in TMS-induced RSFC changes. As expected, TMS over the right PPC caused a rightward shift in line bisection judgment and increased RSFC between the right PPC and the left superior temporal gyrus. This effect was inversely related to FA in the posterior corpus callosum. Local inhibition of the right PPC reshapes connectivity in the attentional network and depends on interhemispheric connections.

neuroscience↗

Oxidative Modifications of Parkin Underlie its Selective Neuroprotection in Adult Human Brain

The mechanisms by which Parkinson disease-linked parkin confers neuroprotection of human dopamine cells remain elusive. We hypothesized that its cysteines mediate multiple anti-oxidant effects in the midbrain. By studying >60 control specimens, we found that in adult human brain - but not in skeletal muscle- parkin is mostly aggregated and insoluble due to oxidative modifications, such as at C253. In vitro, parkins oxidation directly reduces hydrogen peroxide (H2O2) to water. In parkin-deficient human brain, H2O2 concentrations are elevated. In dopamine toxicity studies, wild-type parkin -but not disease-associated mutants-prevents neural death by lowering H2O2 and sequestering radicals within insoluble aggregates. Parkin conjugates dopamine metabolites at the human-specific residue C95 and augments melanin formation in vitro. Using epitope-mapped antibodies, we found that in adult Substantia nigra neurons parkin localizes to neuromelanin within LAMP-3/CD63-positive lysosomes. We conclude that parkins own oxidation, previously considered a loss-of-function event, underlies three neuroprotective effects in adult midbrain: its cysteines participate in H2O2 reduction, dopamine radical conjugation and the formation of neuromelanin.

neuroscience↗

Beyond financial conflicts of interest: Institutional oversight of faculty consulting agreements at schools of medicine and public health

ImportanceApproximately one-third of U.S. life sciences faculty engage in industry consulting. Despite reports that consulting contracts often impinge on faculty and university interests, institutional approaches to regulating consulting agreements are largely unknown.\n\nObjectiveTo investigate the nature of institutional oversight of faculty consulting contracts at U.S. schools of medicine and public health.\n\nDesignStructured telephone interviews with institutional administrators. Questions included the nature of oversight for faculty consulting agreements, if any, and views about consulting as a private versus institutional matter. Interviews were analyzed using a structured coding scheme.\n\nSettingAll accredited schools of medicine and public health in the U.S.\n\nParticipantsAdministrators responsible for faculty affairs were identified via internet searches and telephone and email follow-up. The 118 administrators interviewed represented 73% of U.S. schools of medicine and public health, and 75% of those invited to participate.\n\nInterventionStructured, 15-30 minute telephone interviews.\n\nMain outcomes and measuresPrevalence and type of institutional oversight; responses to concerning provisions in consulting agreements; perceptions of institutional oversight.\n\nResultsOne third of institutions (36%) required faculty to submit at least some agreements for institutional review and 36% reviewed contracts upon request, while 35% refused to review contracts. Among institutions with review, there was wide variation the issues covered. The most common topic was intellectual property rights (64%), while only 23% looked at publication rights and 19% for inappropriately broad confidentiality provisions. Six in ten administrators reported they had no power to prevent faculty from signing consulting agreements. Although most respondents identified institutional risks from consulting relationships, many maintained that consulting agreements are \"private.\"\n\nConclusions and relevanceOversight of faculty consulting agreements at U.S. schools of medicine and public health is inconsistent across institutions and usually not robust. The interests at stake suggest the need for stronger oversight.

scientific communication and education↗