Untargeted lipidomics (Data S1) and targeted metabolomics (Data S2) analysis from in vitro culture of a murine macrophage cell line expressing shRNA targeted to Cardiolipin synthase (CRLS1), referred to as CRLS1 knockdown (KD), or a paired non-target shRNA-expressing (NT-Control). CRLS1 KD and NT-Control macrophages were either directly analyzed (untargeted lipidomics) or stimulated with lipopolysaccharide for a variety of timepoints and then analyzed (targeted metabolomics). Datasets are available as .csv files.
Reynolds M.B. et al. (2023). Cardiolipin coordinates inflammatory metabolic reprogramming through regulation of Complex II disassembly and degradation. Science Advances, 9(5). DOI: 10.1126/sciadv.ade8701
The data and scripts are meant to show how burster dynamics determine response to a single biphasic stimulus. The files include data which show trends in the propensity of termination for different burster types and the MATLAB scripts used to generate this data. The MATLAB scripts also allow the user to generate their own data sets for alternative bursting paths and stimulus parameter combinations. Furthermore, they allow the user to visually examine the effects of single stimuli in the voltage timeseries and in state space. How the user can access these features of the script is described in the file "ReadMe.pdf."
The characterization of HFO networks through functional connectivity analysis and network centrality. Details of the code repository can be found in the README.txt file.
The search data supports a literature review project on Psychological Functioning in Pediatric Patients with Single Ventricle Congenital Heart Disease. The data included are the reproducible search strategies (txt file) and the exported results of all citations from all databases (txt, ris, and.nbib files). Both the original search files and updated search files have been included in the deposit.
Research Overview: This dataset is clinical consent forms, collected as part of Dr. Elizabeth Umberfield's dissertation research of at the University of Michigan. 134 consent forms are used in the analysis, 102 of which are shared here (not all are shared due to data protection agreements with participating sites). The research aimed to enable representation of clinical consent forms and their permissions within the Informed Consent Ontology. These efforts were supported by the Rackham Graduate Student Research Grant, and Dr. Umberfield's doctoral training was supported by the Robert Wood Johnson Foundation Future of Nursing Scholars Program.
Umberfield, E., Jiang, Y., Fenton, S., Stansbury, C., Ford, K., Crist, K., Kardia, S., Thomer, A., & Harris, M. R. (In Press). Lessons Learned for Identifying and Annotating Permissions in Clinical Consents. Applied Clinical Informatics. and Umberfield, E., Stansbury, C., Ford, K., Jiang, Y., Kardia, S. L. R., Thomer, A., & Harris, M. R. (Under Review). Evaluating and Extending the Informed Consent Ontology for Representing Permissions from the Clinical Domain.
These data were produced from the survival analysis of the pre-treatment metabolomics data generated from the Phase II clinical trial of L-carnitine treatment for septic shock (the RACE trial - see https://clinicaltrials.gov/ct2/show/NCT01665092). The results based on respective acetylcarnitine or valine concentration are presented (pdf). The csv files contain the at risk numbers from the Kaplan-Meier survival analysis. These findings described in our manuscript: Pharmacometabolomics Identifies Candidate Predictor Metabolites of an L-carnitine Treatment Mortality Benefit in Septic Shock. and All of the metabolomics data are available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org which is supported by NIH grant U2C-DK119886 and where it has been assigned Project ID (accession number ST001319). The data can be accessed directly via its Project DOIs: (DOI: http://dx.doi.org/10.21228/M8VX0Z).
Puskarich, M. A., Jennaro, T. S., Gillies, C. E., Evans, C. R., Karnovsky, A., McHugh, C. E., Flott, T. L., Jones, A. E., Stringer, K. A., & Investigators, O. behalf of the R. T. (2021). Pharmacometabolomics Identifies Candidate Predictor Metabolites of an L-carnitine Treatment Mortality Benefit in Septic Shock. (Preprint) https://doi.org/10.1101/2021.01.28.21250687
Crouzon FGFR2-C342Y/+ and wild type littermate pups on a C57BL/6 congenic background were injected with lentivirus expressing recombinant TNAP enzyme or phosphate buffered saline shortly after birth. Mice were euthanized 3 weeks after birth for analyses.
Nam, H. K., Vesela, I., Schutte, S. D., & Hatch, N. E. (2020). Viral delivery of tissue nonspecific alkaline phosphatase diminishes craniosynostosis in one of two FGFR2C342Y/+ mouse models of Crouzon syndrome. PLOS ONE, 15(5), e0234073. https://doi.org/10.1371/journal.pone.0234073
The main goal of this research was to identify potential molecular pathways that contribute to memory dysregulation and decline that persists long after illness or inflammation. We have previously established a subchronic immune challenge model that results in memory impairments months after the inflammatory challenge. This project aimed to determine whether memory impairments were accompanied by transcriptional dysregulation in memory related brain region (the hippocampus).
These data show the differential gene expression as log2fold change (and p-value) in males and females 3 months after immune challenge (Supp Tables 1 and 2); after a subsequent immune challenge (Supp Tables 3 and 4); the differential regulation of genes in males and females (Supp Table 5); genes differentially expressed in the hippocampus of males and females at baseline (Supp Table 6) and the differential regulation of those genes in males and females after immune challenge (Supp Tables 7,8).
Tchessalova, D., & Tronson, N. C. (2019). Enduring and sex-specific changes in hippocampal gene expression after a subchronic immune challenge. BioRxiv, 566570. https://doi.org/10.1101/566570
The data and the scripts are to show that seizure onset dynamics and evoked responses change over the progression of epileptogenesis defined in this intrahippocampal tetanus toxin rat model. All tests explored in this study can be repeated with the data and scripts included in this repository. and Dataset citation: Crisp, D.N., Cheung, W., Gliske, S.V., Lai, A., Freestone, D.R., Grayden, D.B., Cook, MJ., Stacey, W.C. (2019). Epileptogenesis modulates spontaneous and responsive brain state dynamics [Data set]. University of Michigan Deep Blue Data Repository. https://doi.org/10.7302/r6vg-9658
Crisp, D. N., Cheung, W., Gliske, S. V., Lai, A., Freestone, D. R., Grayden, D. B., Cook, M. J., & Stacey, W. C. (2020). Quantifying epileptogenesis in rats with spontaneous and responsive brain state dynamics. Brain Communications, 2(1). https://doi.org/10.1093/braincomms/fcaa048
Data include variables used to run accelerated failure time models examining the association between the nose/throat microbiome and 1) symptom duration, 2) shedding duration, and 3) time to infection. Certain individual participant data have been excluded due to identifiability concerns. Data also include the oligotype count table and taxonomic classifications.
Lee KH, Gordon A, Shedden K, Kuan G, Ng S, Balmaseda A, Foxman B. The respiratory microbiome and susceptibility to influenza virus infection. PloS One. 2019;14:e0207898. https://doi.org/10.1371/journal.pone.0207898