Washington University School of Medicine in St. Louis Showcase

Experimental data demonstrating successful propagation of a human gut-associated picobirnavirus in bacterial cells, and thus proving the picobirnavirus is an RNA phage. Data were generated from germ-free mice and bacterial cell community cultures. A total of 68 files were provided, including qPCR/qRT-PCR, flow cytometry, fluorescence microscopy, and sequencing data.

In this study, we found that infection with two unrelated RNA viruses reduced amyloid-beta plaque burden in a mouse model of amyloidosis. There is 1 Excel file containing all raw data generated from mice.

This dataset contains multimodal neuroscience data collected from 25 adult Thy1-GCaMP transgenic mice (~8–12 months of age) undergoing photothrombotic (PT) stroke, generated to assess functional and behavioral changes at acute and chronic timepoints following ischemic injury. Data were acquired from a single biological source — live mice — with tissue samples subsequently processed for post-mortem histological analysis. Three data modalities are included: widefield calcium imaging (WFCI) capturing cortex-wide neural activity via the genetically encoded calcium indicator GCaMP; behavioral data from the cylinder rearing test, which quantifies forelimb asymmetry as a measure of sensorimotor deficit; and histological data comprising both Cresyl Violet (Nissl) staining for lesion visualization and immunohistochemistry (IHC) for protein-specific labeling. Each mouse was assessed at three experimental timepoints: baseline (pre-stroke), acute (24 hours post-PT stroke), and chronic (one week post-PT stroke), with histology collected only at the post-chronic endpoint. The dataset is hierarchically organized under a top-level /data directory containing three primary modality folders: /behavior, /WFCI, and /histology. The /behavior folder is organized by mouse ID (e.g., /M01) and then by timepoint (/bsl, /acute, /weekone), containing raw video recordings, Excel-format scoring sheets, and aggregated GraphPad Prism files summarizing results across all animals. The /WFCI folder is subdivided into three processing tiers — /Raw (unprocessed imaging files), /Tier1_Derived (intermediate processed data), and /Tier2_SourceData (analysis-ready outputs organized by mouse and timepoint) — supporting reproducibility from raw acquisition through final analysis. The /histology folder contains two subfolders, /cresyl_violet and /IHC, holding stained tissue section images. File formats include TIFF images for histology, CSV and XLSX for behavioral scoring, and standard video formats for raw behavior recordings. The organizational rationale — mouse ID → modality → timepoint — enables straightforward longitudinal comparisons within subjects and cross-sectional comparisons across the cohort. Data were generated by Jake Lee and Arnav Ajay Jadav in the Landsness Lab, Department of Neurology, Washington University in St. Louis (contact: jake.l@wustl.edu), and are suitable for analyses of stroke-induced changes in cortical dynamics, motor behavior, and structural pathology.

The purpose of this project is to transform an existing, university-based Long COVID clinic into a broader Long COVID community network in order to expand equitable access to care, improve the patient care experience, and support primary care practitioners in the St. Louis metropolitan area and surrounding rural region. De-identified raw survey response data are shared for patients who explicitly consent to this type of sharing. Similarly, for participants who explicitly consent, de-identified interview transcripts are also shared after redacting potentially unique or identifying information. The files include qualitative data codebooks, REDCap data dictionaries, interview guides and protocols, patient and provider survey, analytic code, administrative codebooks, self report codebook. For survey data, REDCap data dictionaries, surveys, survey administration protocols, a codebook of coded variables are shared. Codebooks contains references and scoring information for relevant survey measures or indicate when survey items were developed or adapted specifically for this study. For each variable in the dataset, the codebook specifies the variable name, variable label/content, response values and labels, and any codes for missing values including numeric values and labels (e.g., 99 = don’t know). For interview data, shared items include interview guides and protocols (including description of interview settings and procedures); general descriptions of interviewers and interviewees (including eligibility criteria, sampling criteria, and recruitment methods); dates interviews were conducted; and codebooks containing code names, labels, and any procedural notes. The collection of this data was conducted with the approval of the Washington University in St. Louis Institutional Review Board (ID# 202401001).

This dataset contains quantitative summary data supporting the publication “Direct activation of SARM1 by dsDNA is not supported by biochemical and cellular evidence.” The data include biochemical and biophysical measurements of purified human SARM1 activity and nucleic acid interactions, including NMR, LC-MS/MS, HPLC, fluorescence-based enzymatic assays, electrophoretic mobility shift assays, mass photometry, size-exclusion chromatography, microscale thermophoresis, and electron microscopy; cell-based measurements of NAD+ metabolism, ATP content, and viability in HEK293T cell lines; and axon degeneration and fluorescence imaging assays in primary mouse dorsal root ganglion neurons. These data were used to generate the quantitative results presented in Figures 1–4 and associated supplemental figures and support the study’s evaluation of whether double-stranded DNA directly activates SARM1, the role of PARP-dependent NAD+ depletion in dsDNA-induced cellular stress, and the functional consequences of the SARM1 3KE mutant. The experimental sources include purified recombinant human SARM1 proteins, human HEK293T cell lines, and primary dorsal root ganglion neurons from wild-type and Sarm1-knockout mice.

In this study, we present amyloid-β-specific engineered CD4+ CAR-T as an approach to directly target sites of pathology. The data is presented in a single spreadsheet file containing all raw data for main and supplementary figures.

In this study we showed that local lentiviral delivery of miR-181a/b-1 enhanced ulnar fracture repair in male and female mice, and in vitro osteogenesis in human cartilage precursor cells. Mechanistically, miR-181a/b-1 directly targeted and suppressed pyruvate dehydrogenase kinase 4 (PDK4), thereby increasing mitochondrial respiration. Consistent with this mechanism, treatment with the PDK4 inhibitor diisopropylamine dichloroacetate (DADA) increased osteogenesis and mitochondrial metabolism in vitro and enhanced endochondral fracture repair in vivo, recapitulating the effects of miR-181a/b-1. This dataset comprises 35 .csv files, providing data related to Figures 2, 3, 4, 5, 6, S9 and S12.

This dataset includes raw z-stack files from the Nikon microscope as well as deleted-slices versions of some of them, and Imaris files for which the original microscope z-stacks are not available. These correspond to the images and movies in the manuscript "Longitudinal single-axon-resolution imaging of peripheral nerve injury response in mice using an optical window implant". The experimental conditions and other information about the images is in the manuscript and the file metadata.

This collection brings together the Knight Alzheimer Disease Research Center (ADRC) Data Freeze datasets published through Digital Commons Data@Becker. Each Data Freeze represents a distinct snapshot of the ADRC research data available at a specific point in time. Individual Data Freeze datasets are assigned separate DOIs to preserve versioned releases, while this collection provides a single entry point for browsing the complete series.

This dataset provides supporting data for the manuscript titled "Chronic oral cannabidiol delays seizure onset and reduces seizure burden in a mouse model of CLN2 disease" and is deposited to comply with PLOS One data availability requirements. The data shows that chronic treatment with cannabidiol confers significant anti-seizure benefit to the mouse model of CLN2 disease, and that it does not appear to do so by altering the inflammatory and neuroimmune markers traditionally used to track CLN2 disease progression. There are four files corresponding to Figures 1 to 3 and Table S1.