About

Ronald Davis is a Professor of Biochemistry and of Genetics at Stanford University. He is affiliated with the Center for Artificial Intelligence in Medicine & Imaging (AIMI) at Stanford. His research focuses on the intersection of artificial intelligence, medicine, and imaging, contributing to advancements in these fields through his leadership and expertise. Davis's work involves applying AI techniques to healthcare challenges, supporting the development of innovative solutions in medical imaging and diagnostics.

Research topics

• Computer Science
• Medicine
• Bioinformatics
• Materials science
• Physical therapy
• Immunology
• Biology
• Internal medicine
• Psychiatry
• Nanotechnology
• Pathology
• Pharmacology
• Embedded system

Selected publications

• 3D ECM-inflammation model on a microfluidic chip for neutrophil transmigration from whole blood investigations

  Lab on a Chip · 2026-01-01

  articleOpen accessSenior author

  of 0.88. Our findings highlight the potential of our platform to facilitate and improve the understanding of neutrophil migration and invasion in inflammation resolution, diseases, and treatments.

  PublisherDOI

• Strontium Aluminosilicate With Surface Nucleated, Crystalline Clad Layer and Amorphous Core

  Journal of the American Ceramic Society · 2026-02-01

  article

  ABSTRACT Surface nucleation and inward crystal growth in 45% SiO 2 – 27.5% Al 2 O 3 – 27.5 SrO (in mol%) glass can be used to create a composite structure with an amorphous core and crystalline clad. The lack of expansion mismatch between the amorphous precursor glass (5.76 ppm/°C) and the fully crystalline material (5.75 ppm/°C) facilitates the formation of mechanically robust structures having a crystalline clad and glassy core. Vickers indentation is used to show that the columnar crystals in the surface clad layer provide a mechanically advantaged structure, i.e., a tortuous path for radial crack extension with crack deflection angles approaching 90°. The optical properties are tunable within this composite material by limiting the depth of the crystalline clad layer to maximize the volume of optically advantaged amorphous material. In an 800 µm thick specimen with a crystalline cladding layer thickness of 130 µm, the axial and diffuse transmittance approach the values obtained for a fully amorphous sample.

  PublisherDOI

• P446 – Venous thromboembolism after radical cystectomy: Incidence, risk factors, and role of anticoagulation

  European Urology · 2025-03-01

  article
  PublisherDOI

• Virus Genome Sequences in the Blood of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients

  medRxiv · 2025-11-07

  preprintOpen accessSenior author

  Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a baffling disease. The disease has a wide spectrum of severity, to date has no established molecular marker, no known causation, and no cure. Many patients report in retrospect that they suffered a virus infection prior to suffering their first symptoms of ME/CFS. Therefore, we report a search for virus genome sequences in the cell-free blood of ME/CFS patients and healthy controls. We used a panel of molecular probes to assess the presence or absence of 185 diverse human viruses in each sample. We identified a total of seventeen viruses, with more in the healthy controls than in the ME/CFS patients.

  PublisherOA PDFDOI

• Light-orchestrated microdroplet reactors for enhanced solid-phase synthesis

  2025-03-19

  article
  PublisherDOI

• Light-orchestrated multi-step solid-phase picodroplet reactors

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-30

  preprintOpen access

  Picoliter droplet reactors, enabled by droplet microfluidics, are revolutionary tools for biochemical reactions with high efficiency, precision, and minimal reagent use. They excel in single-step reactions and reagent addition through droplet merging. Integrating reagent exchange and washing capabilities directly into these platforms may enable complex multi-step processes, such as de novo oligonucleotide synthesis and multiplex immunoassays. However, current picodroplet microfluidics, lacking such capabilities, remain critically deficient in executing multi-step processes. Here we introduce light-orchestrated solid-phase picodroplet reactors to overcome these limitations. Our platform employs optoelectronic tweezers to manipulate individual picodroplets and microbeads. Using this platform, we demonstrate an eight-step click chemistry-based DNA ligation synthesis cycle, with real-time in situ fluorescence detection of reaction products. This platform overcomes single-step limitations by achieving precise sequential encapsulation and decapsulation of beads with different reagent droplets, ensuring uniform reagent exposure and effective washing. Hence it mitigates reaction errors caused by nonuniform reagent exposure and trapped impurities in conventional bulk processing of microbeads. With minimal reagent consumption, real-time analysis, and programmable light- based control, the platform can potentially be scaled and fully automated into a universal and versatile picoliter-scale reagent handling robot for miniaturizing and streamlining workflows in synthetic biology, drug discovery, and beyond.

  PublisherOA PDFDOI

• Oxidative stress is a shared characteristic of ME/CFS and Long COVID

  Proceedings of the National Academy of Sciences · 2025-07-08 · 20 citations

  articleOpen access

  Over 65 million individuals worldwide are estimated to have Long COVID (LC), a complex multisystemic condition marked by fatigue, post-exertional malaise, and other symptoms resembling myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). With no clinically approved treatments or reliable diagnostic markers, there is an urgent need to define the molecular underpinnings of these conditions. By studying bioenergetic characteristics of peripheral blood lymphocytes in 25 healthy controls, 27 ME/CFS, and 20 LC donors, we find both ME/CFS and LC donors exhibit signs of elevated oxidative stress, especially in the memory subset. Using a combination of flow cytometry, RNA-seq, mass spectrometry, and systems chemistry analysis, we observed aberrations in reactive oxygen species (ROS) clearance pathways including elevated glutathione levels, decreases in mitochondrial superoxide dismutase protein levels, and glutathione peroxidase 4-mediated lipid oxidative damage. Strikingly, these redox pathways changes show sex-specific trends. While ME/CFS females exhibit higher total ROS and mitochondrial calcium levels, males have normal ROS levels, with pronounced mitochondrial lipid oxidative damage. In females, these higher ROS levels correlate with T cell hyperproliferation, consistent with the known role of elevated ROS in initiating proliferation. This hyperproliferation can be attenuated by metformin, suggesting this Food and Drug Administration (FDA)-approved drug as a possible treatment, as also suggested by a recent clinical study of LC patients. Moreover, these results suggest a shared mechanistic basis for the systemic phenotypes of ME/CFS and LC, which can be detected by quantitative blood cell measurements, and that effective, patient-tailored drugs might be discovered using standard lymphocyte stimulation assays.

  PublisherOA PDFDOI

• A network medicine approach to investigating ME/CFS pathogenesis in severely ill patients: a pilot study

  Frontiers in Human Neuroscience · 2025-02-10 · 3 citations

  articleOpen access

  This pilot study harnessed the power of network medicine to unravel the complex pathogenesis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). By utilizing a network analysis on whole genome sequencing (WGS) data from the Severely Ill Patient Study (SIPS), we identified ME/CFS-associated proteins and delineated the corresponding network-level module, termed the SIPS disease module, together with its relevant pathways. This module demonstrated significant overlap with genes implicated in fatigue, cognitive disorders, and neurodegenerative diseases. Our pathway analysis revealed potential associations between ME/CFS and conditions such as COVID-19, Epstein-Barr virus (EBV) infection, neurodegenerative diseases, and pathways involved in cortisol synthesis and secretion, supporting the hypothesis that ME/CFS is a neuroimmune disorder. Additionally, our findings underscore a potential link between ME/CFS and estrogen signaling pathways, which may elucidate the higher prevalence of ME/CFS in females. These findings provide insights into the pathogenesis of ME/CFS from a network medicine perspective and highlight potential therapeutic targets. Further research is needed to validate these findings and explore their implications for improving diagnosis and treatment.

  PublisherOA PDFDOI

• Patient-reported treatment outcomes in ME/CFS and long COVID

  Proceedings of the National Academy of Sciences · 2025-07-08 · 14 citations

  articleOpen access

  Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and long COVID are persistent multisystem illnesses affecting many patients. With no known effective FDA-approved treatments for either condition, patient-reported outcomes of treatments may prove helpful in identifying management strategies that can improve patient care and generate new avenues for research. Here, we present the results of an ME/CFS and long COVID treatment survey with responses from 3,925 patients. We assess the experiences of these patients with more than 150 treatments in conjunction with their demographics, symptoms, and comorbidities. Treatments with the greatest perceived benefits are identified. Patients with each condition who participated in the study shared similar symptom profiles, including all the core symptoms of ME/CFS, e.g., 89.7% of ME/CFS and 79.4% of long COVID reported postexertional malaise (PEM). Furthermore, treatment responses between these two patient groups were significantly correlated (R 2 = 0.68). Patient subgroups, characterized by distinct symptom profiles and comorbidities, exhibited increased responses to specific treatments, e.g., a POTS-dominant cluster benefiting from autonomic modulators and a cognitive-dysfunction cluster from CNS stimulants. This study underscores the symptomatic and therapeutic similarities between ME/CFS and long COVID and highlights the commonalities and nuanced complexities of infection-associated chronic diseases and related conditions. While this study does not provide recommendations for specific therapies, in the absence of approved treatments, insights from patient-reported experiences provide urgently needed real-world evidence for developing targeted patient care therapies and future clinical trials.

  PublisherOA PDFDOI

• Tandem metabolic reaction–based sensors unlock in vivo metabolomics

  Proceedings of the National Academy of Sciences · 2025-02-27 · 3 citations

  articleOpen accessCorresponding

  Mimicking metabolic pathways on electrodes enables in vivo metabolite monitoring for decoding metabolism. Conventional in vivo sensors cannot accommodate underlying complex reactions involving multiple enzymes and cofactors, addressing only a fraction of enzymatic reactions for few metabolites. We devised a single-wall-carbon-nanotube-electrode architecture supporting tandem metabolic pathway-like reactions linkable to oxidoreductase-based electrochemical analysis, making a vast majority of metabolites detectable in vivo. This architecture robustly integrates cofactors, self-mediates reactions at maximum enzyme capacity, and facilitates metabolite intermediation/detection and interference inactivation through multifunctional enzymatic use. Accordingly, we developed sensors targeting 12 metabolites, with 100-fold-enhanced signal-to-noise ratio and days-long stability. Leveraging these sensors, we monitored trace endogenous metabolites in sweat/saliva for noninvasive health monitoring, and a bacterial metabolite in the brain, marking a key milestone for unraveling gut microbiota-brain axis dynamics.

  PublisherOA PDFDOI

Recent grants

• Mechanisms of Aging in C. elegans

  NIH · $3.1M · 2007–2021

• NIH Grant R01HG000198

  NIH · $5.2M · 2002

• NIH Grant R01HG001707

  NIH · $1.8M · 2000

• NIH Grant R01GM021891

  NIH · $1.1M · 1988

• NIH Grant R01GM068717

  NIH · $6.5M · 2016

Frequent coauthors

• Wenzhong Xiao

  Harvard University

  209 shared

• Ronald G. Tompkins

  Massachusetts General Hospital

  172 shared

• Lyle L. Moldawer

  Florida College

  115 shared

• Richard Smith

  Pacific Northwest National Laboratory

  98 shared

• David Camp

  Pacific Northwest National Laboratory

  98 shared

• David N. Herndon

  Joseph M. Still Research Foundation

  93 shared

• Weijun Qian

  91 shared

• Michael Mindrinos

  Immucor (United States)

  81 shared