A Roadmap from Single-Cell Transcriptome to Patient Classification for the Immune Response to Trauma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA683058 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR13209400.fastq.gz | Fastqsanger.gz | |||
| SRR13209401.fastq.gz | Fastqsanger.gz | |||
| SRR13209402.fastq.gz | Fastqsanger.gz | |||
| SRR13209403.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 102 |
Similar Datasets
Project description:Immune dysfunction is an important factor driving mortality and adverse outcomes after trauma but remains poorly understood, especially at cellular level. To deconvolute the trauma-induced immune response, we applied single-cell RNA sequencing to circulating and bone marrow mononuclear cells in injured mice and circulating mononuclear cells in trauma patients. In mice, the greatest changes in gene expression were seen in monocytes across both compartments. After systemic injury, the gene expression pattern of monocytes markedly deviated from steady state with corresponding changes in critical transcription factors (TFs), which can be traced back to myeloid progenitors. These changes were largely recapitulated in the human single-cell analysis. We generalized the major changes in human CD14+ monocytes into six signatures, which further defined two trauma patient subtypes (SG1 vs. SG2) identified in the whole blood leukocyte transcriptome in the initial 12h after injury. Compared with SG2, SG1 patients exhibited delayed recovery, more severe organ dysfunction and a higher incidence of infection and non-infectious complications. The two patient subtypes were also recapitulated in burn and sepsis patients, revealing a shared pattern of immune response across critical illness. Our data will be broadly useful to further explore the immune response to inflammatory diseases and critical illness.
2020-12-16 | GSE162806 | GEO
Project description:The mortality rate for patients with trauma is 5.8 million per year. For people aged 15-49, trauma is one of the three leading causes of death. Activation of the coagulation system, intractable hypoxemia, infections and acidosis accompanying post-traumatic patients cannot be separated from trauma immunization. The purpose of this research is to understand the expression of immune cells in patients after trauma, especially severe multiple injuries, and to construct an immune cell profile of patients with multiple injuries.
2022-02-26 | GSE197522 | GEO
Project description:Single cell transcriptical changes in major trauma patient
| PRJNA810736 | ENA
Project description:Background. Coagulopathic bleeding is a major cause of mortality after trauma, and platelet dysfunction contributes to this problem. The causes of platelet dysfunction are relatively unknown, but a great deal can be learned from the plasma environment about the possible pathways involved.
Objective. Describe the changes in plasma proteomic profile associated with platelet dysfunction after trauma.
Methods. Citrated blood was collected from severely injured trauma patients at the time of their arrival to the Emergency Department. Samples were collected from 110 patients, and a subset of twenty-four patients was identified by a preserved (n=12) or severely impaired (n=12) platelet aggregation response to five different agonists. Untargeted proteomics was performed by nanoflow liquid chromatography tandem mass spectrometry. Protein abundance levels for each patient were normalized to total protein concentration to control for hemodilution by crystalloid fluid infusion prior to blood draw.
Results. Patients with platelet dysfunction were more severely injured but otherwise demographically similar to those with retained platelet function. Of 232 proteins detected, twelve were significantly different between groups. These proteins fall into several broad categories related to platelet function, including microvascular obstruction with platelet activation, immune activation, and protease activation.
Conclusions. This observational study provides a description of the change in proteomic profile associated with platelet dysfunction after trauma and identifies twelve proteins with the most profound changes. The pathways involving these proteins are salient targets for immediate investigation to better understand platelet dysfunction after trauma and identify targets for intervention.
2021-02-24 | MSV000086948 | MassIVE
Project description:#G017 Burn/Trauma Study. This is a Glue Grant Study comparison between gene expression analyses performed in eight trauma/burn subjects using either a buffy coat isolation of whole blood or using the PAXgene system Keywords: other
2004-04-24 | GSE1343 | GEO
Project description:Physiological, anatomical, and clinical laboratory analytic scoring systems (APACHE, Injury Severity Score (ISS)) have been utilized, with limited success, to predict outcome following injury. We hypothesized that a peripheral blood leukocyte gene expression score could predict outcome, including multiple organ failure, following severe blunt trauma. Contributor: The Inflammation and the Host Response to Injury Large Scale Collaborative Research Program Keywords: expression profiles cRNA derived from whole blood leukocytes obtained within 12 hours of hospital admission provided gene expression data for the entire genome that were used to create a gene expression score for each patient. Expression profiles from healthy volunteers were averaged to create a reference gene expression profile which was used to compute a difference from reference (DFR) score for each patient. This score described the overall genomic response of patients within the first 12 hours following severe blunt trauma. Regression models were used to compare the association of the DFR, APACHE and ISS scores with outcome.
2009-04-12 | E-GEOD-11375 | biostudies-arrayexpress
Project description:Roadmap Epigenomics Program - UCSF
| PRJNA259584 | ENA
Project description:Roadmap Epigenomics Program - Broad
| PRJNA233641 | ENA
Project description:Acute myocardial infarction (AMI) is accompanied by a systemic trauma response that impacts on the whole body, including blood. In this study, we addressed whether macrophages, key players in trauma repair, sense and respond to these changes. For this, healthy human monocyte-derived macrophages were exposed to 20% human AMI (n=50) or control (n=20) serum and analyzed by transcriptional and multiparameter functional screening followed by network-guided data interpretation and drug repurposing. Results were validated in an independent cohort at functional level (n=47 AMI, n=25 control) and in a public dataset. AMI serum exposure resulted in an overt AMI signature, enriched in debris cleaning, mitosis, and immune pathways. Moreover, we identified gene networks associated with AMI and with poor clinical prognosis in AMI. Network-guided drug screening on the latter unveiled Prostaglandin E2 (PGE2) signaling as target for clinical intervention in detrimental macrophage imprinting during AMI trauma healing. Our results demonstrate pronounced context-induced macrophage reprogramming by the AMI systemic environment, to a degree decisive for patient prognosis. This offers new opportunities for targeted intervention and optimized cardiovascular disease risk management.
2022-12-18 | GSE215801 | GEO
Project description:PTSD - Posttraumatic stress disorder. 33 samples taken from PMBCs of survivors of psychological trauma, in two time points: in ER, few hours after the truma, and four months later. Some of the patients devepled chronic PTSD (17 samples) and others recovered and set to be the Control group (16 samples). This is the normalized active genes: 4512 probes from U95A chip. The raw data is available in series GSE845. Samples are labeled with 3 tags: P/C for PTSD or Control, ER/M4 - for time point of sample, D/ND for Decrement or Non-decrement symptoms over time. (e.g. sample 23C-M4-D-Norm was taken 4 months after trauma from patient 23 which belongs to the control group and showed decrease in symptoms) . Samples include the expression value, the GeneBank accession number and Affymetrix indication of valid calls.
2007-10-03 | E-GEOD-860 | biostudies-arrayexpress