Biology subjects

Xiong, R.

Publications and source records attributed to Xiong, R..

18 recordsLinked to original sources

bioRxiv2026

BCIJelly: An integrated ecosystem for brain-computer interface research

Brain-computer interface (BCI) research relies on multistage computational pipelines, but progress has been slowed by fragmented data formats, heterogeneous decoder implementations and hardware-specific deployment toolchains. Here, we introduce BCIJelly, a unified ecosystem that standardizes 18 BCI datasets into AI-ready inputs and integrates 15 benchmark decoders, 80 reusable modules, automated architecture search (AAS) and hardware-aware neuromorphic deployment. Our AAS constructs task-specific decoders without manual design and extends into a large language model (LLM)-driven closed-loop mode supporting single-task, multitask and cross-species decoder design. A single-command pipeline compiles trained decoders for neuromorphic hardware, reducing power consumption by 30 to 50 times while preserving decoding performance. An interactive visualization software enables code-free exploration of neural recordings and decoding outputs. BCIJelly is validated across five BCI paradigms (motor, visual, speech, emotion and auditory) in humans, macaques and mice, providing an extensible ecosystem connecting data standardization, decoder development, systematic evaluation and hardware-aware deployment for BCI research.

neuroscience↗

bioRxiv2026

An Atlas of Short Linear Motif-Mediated Human Protein-Protein Interactions

Short linear motifs (SLiMs) within intrinsically disordered protein regions mediate transient interactions crucial for cell physiology1. However, the global interaction landscape of human SLiMs remains largely uncharted. Here we present the Atlas of SLiM-mediated Human protein-protein Interactions (ASHI), which maps more than 20,000 interactions by screening over 800 human protein domains against a library of one million peptides tiling the human disordered proteome. ASHI expands the SLiM interactome, uncovers novel binding modes for known peptide-binding domains, and reveals unexpected peptide-binding activities in enzymes, chaperones, RNA-binding proteins, and modification-reader domains. Furthermore, intrinsically disordered regions emerge as densely encoded interaction platforms where interaction specificity is governed by diverse mechanisms, including key motif determinants, flanking residues, competition, and multivalency. These data provide an unprecedented foundation for modeling dynamic interaction networks, interpreting disease-associated variants, and decoding the dark proteome.

biochemistry↗

bioRxiv2026

Gut-derived serine protease reduces sleep but extends lifespan

Sleep has historically been viewed through a brain-centric lens with little known about the contribution of the periphery. Through a targeted screen of secreted peptides from the fat body, gut, and body wall muscle in Drosophila, we identified CG11037, a trypsin-like serine endopeptidase secreted from midgut enterocytes, as a previously unrecognized regulator of sleep. Loss of CG11037 reduces daily sleep, as well as sleep following injury/infection, although recovery is enhanced suggesting reduced need for sleep during sickness. Proteomic analysis of flies with reduced CG11037 revealed altered oxidative stress response pathways including cytochrome P450-related proteins. Indeed, gut-specific knockdown of Cyp6a2 or Cyp28d1 phenocopies CG11037 sleep defects, and loss of CG11037 or P450 elevates reactive oxygen species (ROS) selectively in the gut without affecting brain ROS. Rescue of sleep by antioxidant treatment demonstrates that peripheral ROS accumulation drives the behavioral phenotype. Strikingly, despite physiological dysfunction and reduced sleep, CG11037 or Cytochrome P450 knockdown extends lifespan in a ROS-dependent manner, suggesting that stress adaptation of these knockdowns allows them to live longer. Together, these findings uncover a mechanism for the unexpected association of reduced sleep and extended lifespan.

genetics↗

bioRxiv2026

Endogenous network modeling reveals mechanisms of repair Schwann cell decline and potential recovery targets

Schwann cells, the principal glial cells of the peripheral nervous system, play a central role in nerve repair following injury. Upon injury, mature Schwann cells dedifferentiate into repair Schwann cells. These processes are governed by complex gene regulatory networks, yet the quantitative dynamics of these processes remain unclear. Here, using a bottom-up systems biology approach, we constructed an endogenous regulatory network model based on experimentally validated interactions, without relying on high-throughput data as input. The model captures Schwann cell dedifferentiation dynamics and reveals a potential landscape composed of stable states and intermediate transition states. Simulations recapitulate post-injury trajectories and confirm the role of c-Jun upregulation in maintaining repair capacity. Furthermore, the model predicts multiple potential therapeutic targets, including P53, JNK, and PTEN, for sustaining repair competence. We also identify intrinsic heterogeneity within repair Schwann cells and uncover key transition states that simultaneously connect repair-competent cells to both repair-deficient and apoptotic phenotypes, indicating that these intermediate states may represent critical regulatory bottlenecks and key cellular targets for improving the success of peripheral nerve regeneration. Overall, this work provides new insights into the precise regulation of Schwann cell fate and establishes a theoretical framework for regenerative medicine and clinical strategies in peripheral nerve repair.

neuroscience↗

bioRxiv2026

An apical junction protein antagonizes mechanosensitive calcium signaling to establish stochastic choices of olfactory neuron subtypes

Mechanical forces regulate brain development and left-right body patterning. However, the role of mechanical signaling in brain lateralization remains unclear. In Caenorhabditis elegans, the left and right AWC olfactory neurons communicate via a gap junction network to stochastically differentiate into the default AWCOFF and induced AWCON subtypes. SLO BK potassium channels, SLO-1 and SLO-2, act redundantly to inhibit a calcium-regulated protein kinase pathway in the specification of the AWCON subtype. Here, we identified a role for AJM-1 (apical junction molecule 1) in promoting AWCON from an unbiased forward genetic screen for mutants that suppress the slo-1(gf) 2AWCON phenotype. AJM-1 is located at three distinct tight junctions between amphid neurons (including AWC) and sheath glia, sheath and socket glia, and socket glia and hypodermal cells (also known as epidermal cells) at the anterior tip of the animal. In addition to its cell-autonomous function, the non-cell-autonomous function of AJM-1 in glial and hypodermal cells is required for the specification of the AWCON subtype. Furthermore, we identified a role for the DEL-1 mechanosensitive DEG/ENaC channel in the calcium signaling pathway, mediated by UNC-2 and EGL-19 voltage-activated calcium channels, that specifies AWCOFF. Together, our results suggest a mechanism in which AJM-1 promotes SLO-1 expression and antagonizes mechanosensitive calcium signaling, thereby promoting the AWCON subtype. This study provides insight into the role of mechanical force in the stochastic lateralization of olfactory neurons.

developmental biology↗

bioRxiv2026

Substrate binding and activation mechanism of the essential bacterial septal cell wall synthase FtsW

Septal peptidoglycan (sPG) synthesis in most bacteria is driven by the essential, highly conserved FtsWIOLB synthase complex, comprising the SEDS glycosyltransferase FtsW, the monofunctional transpeptidase FtsI, and the scaffolding subcomplex FtsOLB. Although apo structures of FtsWIOLB are known, no substrate-bound structures exist, likely due to the intrinsic flexibility of lipid II (L2) substrates. Here, we combined all-atom molecular dynamics simulations of E. coli FtsWIOLB with cysteine-based mutagenesis and cell-based assays to define donor and acceptor L2 binding sites in FtsW and to elucidate the complexs activation mechanism. We show that conserved arginine residues adjacent to membrane-accessible cavities in FtsW coordinate donor and acceptor L2 pyrophosphate groups, stabilizing substrate binding. The FtsWIOLB complex appears to adopt a self-inhibitory architecture in which gating elements and a periplasmic loop prevent the donor and acceptor from approaching FtsWs catalytic residue D297. Activation by FtsN or a superfission FtsW variant relieves these constraints, stabilizes acceptor-site binding, and reorients both substrates into a catalytically primed state. Long donor glycan chains further stabilize this activated conformation at the acceptor site, promoting processive sPG polymerization. Comparative modeling of ESKAPE pathogen homologs reveals conserved and divergent features of binding-site engagement and activation. We corroborate these computational findings with cysteine-based mutagenesis and crosslinking experiments. These results establish a mechanistic framework for FtsW substrate recognition and functional activation, highlighting tractable sites for structure and mechanism-based antibiotic discovery targeting SEDS-class cell wall synthases.

biophysics↗

bioRxiv2026

Benchmarking Next-Generation Sequencing Platforms: A Comprehensive Comparison Of Single-Cell RNA-Seq from Ultima UG 100 vs. Illumina NovaSeq X Plus

Single-cell RNA sequencing (scRNA-seq) has become an essential technology for dissecting cellular heterogeneity in complex biological systems, with Illumina platforms serving as the dominant NGS provider1-3. The recent emergence of the Ultima Genomics UG 100 platform offers a high-throughput and potentially more cost-effective alternative, warranting a rigorous comparative analysis. Here, we conducted a comprehensive head-to-head comparison of the Ultima Genomics UG 100 and Illumina NovaSeq X Plus platforms, generating deep-coverage scRNA-seq data from human PBMCs and stimulated T-cell samples. Our multi-level analysis revealed highly concordant performance in both cell type identification and gene expression. We found that both platforms robustly captured all major immune lineages and demonstrated good transcriptional agreement. Minor observed discrepancies were primarily correlated with low UMI counts, suggesting stochastic biological effects rather than technical variance. Overall, our study establishes that the Ultima UG 100 delivers performance highly comparable to the Illumina NovaSeq X Plus for single-cell transcriptomics.

bioinformatics↗

bioRxiv2026

Kinesin-1 trans-synaptically regulates synaptic localization of SARM1 for asymmetric neuron diversification

The Caenorhabditis elegans AWC olfactory neuron pair differentiates stochastically into two distinct subtypes, default AWCOFF and induced AWCON. A calcium signaling complex assembled by the TIR-1/SARM1 adaptor protein is transported from the AWC cell body to the axons, where it cell autonomously specifies the AWCOFF subtype through lateral signaling. UNC-104, the C. elegans homolog of the kinesin-3 motor protein KIF1A, acts non-cell autonomously in AWCON to control the synaptic localization of the TIR-1 signaling complex in promoting AWCOFF. Here, we identify a non-cell-autonomous role of unc-116/kinesin-1, similar to that of unc-104/kinesin-3, in promoting AWCOFF. unc-116 mutants, similar to unc-104 mutants, enhance the 2AWCON phenotype of a hypomorphic tir-1 mutant. Overexpression of unc-116 in AWC causes a 2AWCOFF phenotype, the same as the tir-1 overexpression phenotype. Like UNC-104, UNC-116 plays a non-cell-autonomous role in the AWCON cell to promote AWCOFF cell subtype by regulating the dynamic trafficking of TIR-1 along the AWC axon. UNC-116 is strikingly colocalized with UNC-104, while both are generally adjacent to TIR-1. Taken together, these results suggest a model in which UNC-116/kinesin-1 and UNC-104/kinesin-3 may work cooperatively to transport some unknown presynaptic factor(s) in the future AWCON cell that trans-synaptically regulates the dynamic trafficking of the TIR-1/SARM1 signaling complex to postsynaptic regions of the AWC axons in promoting the AWCOFF subtype.

developmental biology↗

bioRxiv2025

FuzzAletheia: Mapping dynamic interaction landscapes of intrinsically disordered protein-ligand complexes to accelerate ligand optimization

Intrinsically disordered proteins (IDPs), representing more than 30% of human proteome, present great challenges in rational drug design due to their highly flexible conformations and dynamic interactions. Though their malfunction is linked to major diseases, IDPs are difficult to target. A critical roadblock lies in hit-to-lead optimization due to their dynamic interactions with hit compounds. Here we developed FuzzAletheia, an IDP-ligand dynamic binding pattern analyzer, to accelerate hit optimization. It analyzes the molecular dynamics simulation trajectories of IDP-ligand to cluster interactions into distinct spatiotemporal stable binding features, which are then visualized and quantified to provide insights into the dynamic binding orientation, strength, and stability. This analysis pinpoints modification sites on hit compounds for optimization. We applied FuzzAletheia to the disordered p53 transactivation domain 1 and its hit compound 1050. Guided by FuzzAletheia analysis, we designed and synthesized six derivatives of 1050 and the most potent compound achieved a 10-fold enhancement in activity, demonstrating its power to accelerate IDP hit optimization.

biophysics↗

bioRxiv2025

Scavenger Receptor class F member 2 is an intracellular receptor for Hepatitis B virus

Hepatitis B virus (HBV) infects hepatocytes by specific binding to the cell-surface receptor --sodium taurocholate cotransporting polypeptide (NTCP)--through the preS1 region of its large envelop protein, followed by a less well understood transport process across the cytoplasm to the nucleus. Here, we report that scavenger receptor class F member 2 (SCARF2), a single-pass transmembrane protein, functions as an intracellular receptor for HBV. SCARF2 binds to a preS1 region downstream of the NTCP binding site through its N-terminal EGF-like domains 4-6, and its proline-rich C-terminal domain also plays an indispensable role in the infection. The internalized HBV virions are transported to the cytoplasmic side of nuclear pore complexes (NPCs) within the SCARF2-containing endosomes. HBV capsid release from the endosomal vesicles is significantly impaired by knockdown of SCARF2. These results suggest a model that SCARF2 conveys HBV to the periphery of NPCs and ultimately leads to viral capsid release for nuclear entry.

microbiology↗

bioRxiv2024

Quantitative Resolving Cell Fate in the Early Embryogenesis of Caenorhabditis elegans

The nematode Caenorhabditis elegans exhibits an invariant cell lineage during its development where the gene-molecular network that regulates the development is crucial for the biological process. While there are many molecular cell atlases describing the phenomena and key molecules involved in cell transformation, the underlying mechanisms from a systems biology perspective have received less attention. Based on an endogenous molecular-cellular theory that relates the molecular mechanisms to biological phenotypes, we constructed a model of core endogenous network to describe the early stages of embryonic development of the nematode. Different cell types and intermediate cell states during development from zygotes to founder cells correspond to the steady states of the network as a nonlinear stochastic dynamical system. Connections between steady states form a topological landscape that encompasses known developmental lineage trajectories. By regulating the expression of agents in the network, we quantitatively simulated the effects of the Wnt and Notch signaling pathway on cell fate transitions and predicted the possible trajectories of transdifferentiation of the AB cell across the lineage. The success of the current study may help advance our understanding of the fundamental principles of developmental biology and cell fate determination, offering an effective tool for quantitative analysis of cellular processes.

developmental biology↗

bioRxiv2024

BioMapAI: Artificial Intelligence Multi-Omics Framework Modeling of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic illness with a multifactorial etiology and heterogeneous symptomatology, posing major challenges for diagnosis and treatment. Here, we present BioMapAI, a supervised deep neural network trained on a four-year, longitudinal, multi-omics dataset from 249 participants, which integrates gut metagenomics, plasma metabolomics, immune cell profiling, blood laboratory data, and detailed clinical symptoms. By simultaneously modeling these diverse data types to predict clinical severity, BioMapAI identifies disease- and symptom-specific biomarkers and robustly classifies ME/CFS in both held-out and independent external cohorts. Using an explainable AI approach, we construct the first connectivity map spanning the microbiome, immune system, and plasma metabolome in health and ME/CFS, adjusted for age, gender, and additional clinical factors. This map uncovers disrupted associations between microbial metabolism (e.g., short-chain fatty acids, branched-chain amino acids, tryptophan, benzoate), plasma lipids and bile acids, and heightened inflammatory responses in mucosal and inflammatory T cell subsets (MAIT, {gamma}{delta}T) secreting IFN{gamma} and GzA. Overall, BioMapAI provides unprecedented systems-level insights into ME/CFS, refining existing hypotheses and hypothesizing new pathways associated to the diseases heterogeneous symptoms.

bioinformatics↗

bioRxiv2023

Energy Landscape near Glioma Decipher the Role of Glioma Stem Cell within Glioma Hierarchy

Glioma stem cells (GSCs) have been recognized as key players in glioma recurrence and therapeutic resistance, presenting a promising target for novel treatments. However, the limited understanding of the role GSCs play in the glioma hierarchy has drawn controversy and hindered research translation into therapies. Despite significant advances in our understanding of gene regulatory networks, the dynamics of these networks and their implications for glioma remain elusive. This study employs a systemic theoretical perspective to integrate empirical knowledge into a core endogenous network model for glioma, thereby elucidating its energy landscape through network dynamics computation. The model identifies two stable states corresponding to astrocytoma and oligodendroglioma, connected by a transitional state associated with GSCs, indicating the instability of GSCs in vivo and providing negative proof of their role as the cellular origin for glioma. We also obtained various stable states further indicative of gliomas multicellular origins and uncovered a group of transition states that could potentially induce tumor heterogeneity and therapeutic resistance. This research proposes that the transitional states linking both glioma stable states are central to glioma heterogeneity and therapy resistance, suggesting a combination of apoptosis-inducing and differentiation-promoting therapies as a potential strategy. Our approach holds promise for advancing glioma therapy by providing a new lens through which to view the complex landscape of glioma biology.

systems biology↗

bioRxiv2023

Evolution of the Telencephalon Anterior-Posterior Patterning by Core Endogenous Network Bifurcation

How did the complex structure of telencephalon evolve? Existing explanations are based on phenomena and lack the first principle. The Darwinian dynamics and the endogenous network theory established a few years ago provide a mathematical and theoretical framework of a dynamical structure, and a general constitutive structure for theory-experiment coupling, respectively, for answering this question from the first principle perspective. By revisiting a gene network that explains the anterior-posterior patterning of the vertebrate telencephalon, we found that with the increase of the cooperative effect in this network, the fixed points gradually evolve, accompanied by the occurrence of two bifurcations. The dynamic behavior of this network consists with the knowledge obtained from experiments on telencephalon evolution. Furtherly, our work drew an answer quantitatively of how the telencephalon anterior-posterior patterning evolved from the pre-vertebrate chordate to the vertebrate and gave a series of verifiable predictions in a first principle manner. Figure Abstract O_FIG_DISPLAY_L [Figure 1] M_FIG_DISPLAY C_FIG_DISPLAY

systems biology↗

bioRxiv2023

High-Throughput Bioprinting of the Nasal Epithelium using Patient-derived Nasal Epithelial Cells

Human nasal epithelial cells (hNECs) are an essential cell source for the reconstruction of the respiratory pseudostratified columnar epithelium composed of multiple cell types in the context of infection studies and disease modeling. Hitherto, manual seeding has been the dominant method for creating nasal epithelial tissue models. However, the manual approach is slow, low-throughput and has limitations in terms of achieving the intricate 3D structure of the natural nasal epithelium in a uniform manner. 3D Bioprinting has been utilized to reconstruct various epithelial tissue models, such as cutaneous, intestinal, alveolar, and bronchial epithelium, but there has been no attempt to use of 3D bioprinting technologies for reconstruction of the nasal epithelium. In this study, for the first time, we demonstrate the reconstruction of the nasal epithelium with the use of primary hNECs deposited on Transwell inserts via droplet-based bioprinting (DBB), which enabled high-throughput fabrication of the nasal epithelium in Transwell inserts of 24-well plates. DBB of nasal progenitor cells ranging from one-tenth to one-half of the cell seeding density employed during the conventional cell seeding approach enabled a high degree of differentiation with the presence of cilia and tight-junctions over a 4-week air-liquid interface culture. Single cell RNA sequencing of these cultures identified five major epithelial cells populations, including basal, suprabasal, goblet, club, and ciliated cells. These cultures recapitulated the pseudostratified columnar epithelial architecture present in the native nasal epithelium and were permissive to respiratory virus infection. These results denote the potential of 3D bioprinting for high-throughput fabrication of nasal epithelial tissue models not only for infection studies but also for other purposes such as disease modeling, immunological studies, and drug screening.

bioengineering↗

bioRxiv2022

The mechanism of nicotinamide phosphoribosyltransferase whereby positive allosteric modulation elevates cellular NAD+

In aging and disease, cellular NAD+ is depleted by catabolism to nicotinamide (NAM) and NAD+ supple-mentation is being pursued to enhance human healthspan and lifespan. Activation of nicoti namide phosphoribosyl -transferase (NAMPT), the rate-limiting step in NAD+ biosynthesis, has potential to increase salvage of NAM. Novel NAMPT positive allosteric modulators (N-PAMs) were discovered in addition to demonstration of NAMPT activati on by biogenic phenols. The mechanism of activation was revealed through synthesis of novel chemical probes, new NAMPT co-crystal structures, and enzyme kinetics. Binding to a rear channel in NAMPT regulates NAM binding and turnover, with biochemical observations being replicated by NAD+ measurements in human cells. The mechanism of action of N-PAMs identifies, for the first time, the role of the rear channel in regulation of NAMPT turnover coupled to feedback inhibition by NAM. N-PAM inhibition of low affinity, non-productive NAM binding via the rear channel, causes a right-shif t in KI(NAM) that accompanies an increase in enzyme activity. Conversion of an N-PAM to a high-affinity l igand blocks both high and low affinity NAM binding, ablating enzyme activity. In the presence of an N-PAM, NAMPT boosts NAD+ biosynthesis at higher NAM concentrations, in addition to relieving inhibition by NAD+. Since cellular stress often leads to enhanced catabolism of NAD+ to NAM, this mechanism is relevant to supporting cellular N AD+ levels in aging and disease. The tight regulation of cellular NAMPT is differentially regulated by N-PAMs and other activators, indicating that different classes of pharmacological activators may be engineered for cell and tissue selectivity.

biochemistry↗

bioRxiv2020

Novel and potent inhibitors targeting DHODH, a rate-limiting enzyme in de novo pyrimidine biosynthesis, are broad-spectrum antiviral against RNA viruses including newly emerged coronavirus SARS-CoV-2

Emerging and re-emerging RNA viruses occasionally cause epidemics and pandemics worldwide, such as the on-going outbreak of coronavirus SARS-CoV-2. Existing direct-acting antiviral (DAA) drugs cannot be applied immediately to new viruses because of virus-specificity, and the development of new DAA drugs from the beginning is not timely for outbreaks. Thus, host-targeting antiviral (HTA) drugs have many advantages to fight against a broad spectrum of viruses, by blocking the viral replication and overcoming the potential viral mutagenesis simultaneously. Herein, we identified two potent inhibitors of DHODH, S312 and S416, with favorable drug-like and pharmacokinetic profiles, which all showed broad-spectrum antiviral effects against various RNA viruses, including influenza A virus (H1N1, H3N2, H9N2), Zika virus, Ebola virus, and particularly against the recent novel coronavirus SARS-CoV-2. Our results are the first to validate that DHODH is an attractive host target through high antiviral efficacy in vivo and low virus replication in DHODH knocking-out cells. We also proposed the drug combination of DAA and HTA was a promising strategy for anti-virus treatment and proved that S312 showed more advantageous than Oseltamivir to treat advanced influenza diseases in severely infected animals. Notably, S416 is reported to be the most potent inhibitor with an EC50 of 17nM and SI value >5882 in SARS-CoV-2-infected cells so far. This work demonstrates that both our self-designed candidates and old drugs (Leflunomide/Teriflunomide) with dual actions of antiviral and immuno-repression may have clinical potentials not only to influenza but also to COVID-19 circulating worldwide, no matter such viruses mutate or not.

microbiology↗

bioRxiv2018

Animal models of chemotherapy-induced peripheral neuropathy: a machine-assisted systematic review and meta-analysis A comprehensive summary of the field to inform robust experimental design

Background and aimsChemotherapy-induced peripheral neuropathy (CIPN) can be a severely disabling side-effect of commonly used cancer chemotherapeutics, requiring cessation or dose reduction, impacting on survival and quality of life. Our aim was to conduct a systematic review and meta-analysis of research using animal models of CIPN to inform robust experimental design.\n\nMethodsWe systematically searched 5 online databases (PubMed, Web of Science, Citation Index, Biosis Previews and Embase (September 2012) to identify publications reporting in vivo CIPN modelling. Due to the number of publications and high accrual rate of new studies, we ran an updated search November 2015, using machine-learning and text mining to identify relevant studies.\n\nAll data were abstracted by two independent reviewers. For each comparison we calculated a standardised mean difference effect size then combined effects in a random effects meta- analysis. The impact of study design factors and reporting of measures to reduce the risk of bias was assessed. We ran power analysis for the most commonly reported behavioural tests.\n\nResults341 publications were included. The majority (84%) of studies reported using male animals to model CIPN; the most commonly reported strain was Sprague Dawley rat. In modelling experiments, Vincristine was associated with the greatest increase in pain-related behaviour (-3.22 SD [-3.88; -2.56], n=152, p=0). The most commonly reported outcome measure was evoked limb withdrawal to mechanical monofilaments. Pain-related complex behaviours were rarely reported. The number of animals required to obtain 80% power with a significance level of 0.05 varied substantially across behavioural tests. Overall, studies were at moderate risk of bias, with modest reporting of measures to reduce the risk of bias.\n\nConclusionsHere we provide a comprehensive summary of the field of animal models of CIPN and inform robust experimental design by highlighting measures to increase the internal and external validity of studies using animal models of CIPN. Power calculations and other factors, such as clinical relevance, should inform the choice of outcome measure in study design.

neuroscience↗