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.

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 #
5U24DK059637-13
Application #
8517673
Study Section
Special Emphasis Panel (ZDK1-GRB-S)
Project Start
Project End
Budget Start
2013-06-01
Budget End
2014-05-31
Support Year
13
Fiscal Year
2013
Total Cost
$209,446
Indirect Cost
$75,186
Name
Vanderbilt University Medical Center
Department
Type
DUNS #
004413456
City
Nashville
State
TN
Country
United States
Zip Code
37212
Otero, Yolanda F; Mulligan, Kimberly X; Barnes, Tammy M et al. (2016) Enhanced Glucose Transport, but not Phosphorylation Capacity, Ameliorates Lipopolysaccharide-Induced Impairments in Insulin-Stimulated Muscle Glucose Uptake. Shock 45:677-85
Babaev, Vladimir R; Ding, Lei; Zhang, Youmin et al. (2016) Macrophage IKKα Deficiency Suppresses Akt Phosphorylation, Reduces Cell Survival, and Decreases Early Atherosclerosis. Arterioscler Thromb Vasc Biol 36:598-607
Li, Mingyu; Page-McCaw, Patrick; Chen, Wenbiao (2016) FGF1 Mediates Overnutrition-Induced Compensatory β-Cell Differentiation. Diabetes 65:96-109
Jones, Carissa P; Boyd, Kelli L; Wallace, Jeanne M (2016) Evaluation of Mice Undergoing Serial Oral Gavage While Awake or Anesthetized. J Am Assoc Lab Anim Sci 55:805-810
Hempel, Jonathan E; Cadar, Adrian G; Hong, Charles C (2016) Development of thieno- and benzopyrimidinone inhibitors of the Hedgehog signaling pathway reveals PDE4-dependent and PDE4-independent mechanisms of action. Bioorg Med Chem Lett 26:1947-53
Boortz, Kayla A; Syring, Kristen E; Lee, Rebecca A et al. (2016) G6PC2 Modulates the Effects of Dexamethasone on Fasting Blood Glucose and Glucose Tolerance. Endocrinology 157:4133-4145
Sinha, Seema; Hoshino, Daisuke; Hong, Nan Hyung et al. (2016) Cortactin promotes exosome secretion by controlling branched actin dynamics. J Cell Biol 214:197-213
Ceddia, Ryan P; Lee, DaeKee; Maulis, Matthew F et al. (2016) The PGE2 EP3 Receptor Regulates Diet-Induced Adiposity in Male Mice. Endocrinology 157:220-32
McKenzie, Andrew J; Hoshino, Daisuke; Hong, Nan Hyung et al. (2016) KRAS-MEK Signaling Controls Ago2 Sorting into Exosomes. Cell Rep 15:978-87
Romere, Chase; Duerrschmid, Clemens; Bournat, Juan et al. (2016) Asprosin, a Fasting-Induced Glucogenic Protein Hormone. Cell 165:566-79

Showing the most recent 10 out of 546 publications