Abstract

The Analytical Resources Core is composed of three subcores: 1) Hormone Assay and Analytical Services;2) Lipids and Lipoproteins;and 3) Mouse Pathology. These subcores share resources with others in the Vanderbilt DRTC where they have served to streamline research activities, produce cost-effective lines of experimentation, foster collaborative enterprises, and provide alternative outlets to scientists reaching the technical limits of their own laboratories. The services offered by each subcore are unique in their application to the mouse, and great effort has been made to establish assay specificity and scale down sample size to accommodate samples from this species. The Core provides space, equipment, and personnel for sample analyses and method development. Investigators pay a fee-for-service that covers the cost of reagents, supplies, a percentage of personnel salary, and pro-rated service contracts.

Public Health Relevance

The Analytical Resources Core provides chemical analyses and pathology services for biological specimens obtained from genetic mouse models of diabetes and metabolic disease. The services provided by this Core are essential to understanding the specific genes that underlie these conditions.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Resource-Related Research Projects--Cooperative Agreements (U24)
Project #
5U24DK059637-14
Application #
8708036
Study Section
Special Emphasis Panel (ZDK1-GRB-S)
Project Start
Project End
Budget Start
2014-06-01
Budget End
2015-05-31
Support Year
14
Fiscal Year
2014
Total Cost
$217,041
Indirect Cost
$77,912

  Institution

Name
Vanderbilt University Medical Center
Department
Type
DUNS #
004413456
City
Nashville
State
TN
Country
United States
Zip Code
37212

  Publications

Williams, Ian M; Valenzuela, Francisco A; Kahl, Steven D et al. (2018) Insulin exits skeletal muscle capillaries by fluid-phase transport. J Clin Invest 128:699-714
Hughey, Curtis C; Trefts, Elijah; Bracy, Deanna P et al. (2018) Glycine N-methyltransferase deletion in mice diverts carbon flux from gluconeogenesis to pathways that utilize excess methionine cycle intermediates. J Biol Chem 293:11944-11954
Kook, Seunghyi; Qi, Aidong; Wang, Ping et al. (2018) Gene-edited MLE-15 Cells as a Model for the Hermansky-Pudlak Syndromes. Am J Respir Cell Mol Biol 58:566-574
Yao, Lina; Seaton, Sarah Craven; Ndousse-Fetter, Sula et al. (2018) A selective gut bacterial bile salt hydrolase alters host metabolism. Elife 7:
Babaev, Vladimir R; Huang, Jiansheng; Ding, Lei et al. (2018) Loss of Rictor in Monocyte/Macrophages Suppresses Their Proliferation and Viability Reducing Atherosclerosis in LDLR Null Mice. Front Immunol 9:215
Pollins, Alonda C; Boyer, Richard B; Nussenbaum, Marlieke et al. (2018) Comparing Processed Nerve Allografts and Assessing Their Capacity to Retain and Release Nerve Growth Factor. Ann Plast Surg 81:198-202
Harris, Nicholas A; Isaac, Austin T; Günther, Anne et al. (2018) Dorsal BNST ?2A-Adrenergic Receptors Produce HCN-Dependent Excitatory Actions That Initiate Anxiogenic Behaviors. J Neurosci 38:8922-8942
Fensterheim, Benjamin A; Young, Jamey D; Luan, Liming et al. (2018) The TLR4 Agonist Monophosphoryl Lipid A Drives Broad Resistance to Infection via Dynamic Reprogramming of Macrophage Metabolism. J Immunol 200:3777-3789
Ehrlicher, Sarah E; Stierwalt, Harrison D; Newsom, Sean A et al. (2018) Skeletal muscle autophagy remains responsive to hyperinsulinemia and hyperglycemia at higher plasma insulin concentrations in insulin-resistant mice. Physiol Rep 6:e13810
Mani, Bharath K; Castorena, Carlos M; Osborne-Lawrence, Sherri et al. (2018) Ghrelin mediates exercise endurance and the feeding response post-exercise. Mol Metab 9:114-130

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