Summary of Study ST000314

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000253. The data can be accessed directly via it's Project DOI: 10.21228/M8302K This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

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Study IDST000314
Study TitleNSAID treatment alters the metabolomics profile of liver, kidney, lung, and heart in an experimental mouse model of heat stroke
Study TypeMetabolomics
Study SummaryThe objective of this study is to exploit broad spectrum metabolomic analysis to identify new biomarkers of multi-organ damage that will improve heat stroke (HS) diagnosis and treatment. The central hypothesis is that HS will lead to significant alterations in multi-organ metabolomics profiles that will serve as markers of HS severity, which will be shifted and intensified further by the acute use of NSAIDs. To test this hypothesis, we will be performing broad spectrum metabolomics to identify alternations in the metabolic signatures of key organs (heart, liver, kidney, and lung) in a highly validated rodent HS model leveraging implantable radiotelemetry. We will then compare these results with already completed histological gene/protein expression analysis to determine the best metabolic markers of HS induced organ damage. The results from this study will aid in the identification of preventative measures to reduce HS risk, as well as in developing therapeutics to treat multi-organ damage and facilitate recovery. The proposed study will provide the first metabolic assessment of HS severity and NSAID use, which will support future studies in HS patients to validate novel biomarkers that will improve clinical assessment of organ damage and recovery.
Institute
University of North Carolina
DepartmentSystems and Translational Sciences
LaboratorySumner Lab
Last NameSumner
First NameSusan
AddressEastern Regional Comprehensive Metabolomics Resource Core, UNC Nutrition Research Institute, 500 Laureate Way, Kannapolis, NC, 28081
Emailsusan_sumner @unc.edu
Phone704-250-5066
Submit Date2015-12-31
Num Groups83
Raw Data AvailableYes
Raw Data File Type(s)fid
Analysis Type DetailNMR
Release Date2016-12-31
Release Version1
Susan Sumner Susan Sumner
https://dx.doi.org/10.21228/M8302K
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000253
Project DOI:doi: 10.21228/M8302K
Project Title:NSAID treatment alters the metabolomics profile of liver, kidney, lung, and heart in an experimental mouse model of heat stroke
Project Summary:Heat stroke (HS) is a significant medical threat to civilians and those serving in the U.S. Armed forces. The physiological and molecular mechanisms that are critical in HS morbidity and mortality, both during and after HS onset, remain yet to be elucidated. Current clinical biomarkers lack specificity and sensitivity to accurately diagnose HS severity, and there is a critical need for effective pharmacologic interventions and treatments that address this life-threatening disease. The systemic inflammatory response (SIR) is one target for such pharmacological interventions, as it is thought to mediate much of HS etiology. For this reason, anti-inflammatories have been directed at the SIR in an effort to treat and prevent HS. Due to their anti-inflammatory actions, non-steroidal anti-inflammatory drugs (NSAIDS) have been suggested as a treatment candidate for HS. Currently, NSAIDs are one of the most widely used medications across the world, with hundreds of millions of doses prescribed yearly. Of special concern, NSAID use is prolific throughout the U.S. Armed Forces. We recently examin4ed the effect of using NSAIDs to treat HS, and found that NSAIDs actually increase HS mortality and exacerbate the systemic organ damage (e.g., gut, kidneys) found in HS recovery in mice. Our finding suggest the use of NSAIDs by civilians and military populations may increase the risk of HS morbidity and mortality. The objective of this proposal is to exploit broad spectrum metabolomic analysis to identify new biomarkers of multi-organ damage that will improve HS diagnosis and treatment.
Institute:US Army Research Institute
Department:Environmental Medicine
Last Name:Audet;Leon
First Name:Gerald;Lisa
Address:Building 42, Kansas Street, Natick, MA 01760
Email:gerald.n.audet.ctr@mail.mil
Phone:508.233.5959
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