CORE Awill serve as the Administrative and Informatics Core for the Program ProjectGrant. It will assistPPG investigators and Coreleaders by providingnecessary planning and developmentand prepare annualgrant reports. CoreAwill plan and run monthlyPPGresearch rounds,meetings of the InternalSteeringCommittee, and the External Advisory Committee (EAC). CoreAwill work with the EAC to obtain and disseminate evaluations of the program. The core will also meet regulatory requirements as established by federal and state governments. CoreAwill also assist with the preparation of competingand non-competing grant renewals necessary for maintenanceof the PPG. It will provided help with budgets, animalprotocols, human use requirements, toxic chemical information, homelandsecurity requirments, personnelissues, etc. Core Awill provide assistance with travel for seminar and workshop speakers, EAC members, and PPGparticipants. CoreA will also run searches for replacement PPG staff and post-doctoral students as positionsare vacated. The Core will assist with relocation issues for staff, students and post-docs that take positionsin the Program. The core will help with visa and immigration requirements to see that PPGstaff and students remain in compliancewith federal requirements. The Core will provide statistical consultingfor planning of experimentalprotocols and analysis of data.

Public Health Relevance

The PPG is investigating the structure of the neuromuscular apparatus of the Gl tract. This topic is relevant to clinical problems faced by millions of patients. Core A provides centralized administrative support to the investigative team to increase their efficiency. Core A also provides statistical consulting to increase the power of experiments, reduce the use of animals, and increase validity of the findings.

National Institute of Health (NIH)
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Research Program Projects (P01)
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Special Emphasis Panel (ZDK1-GRB-9)
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University of Nevada Reno
United States
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Durnin, Leonie; Kwok, Benjamin; Kukadia, Priya et al. (2018) An ex vivo bladder model with detrusor smooth muscle removed to analyse biologically active mediators released from the suburothelium. J Physiol :
Shi, Junchao; Ko, Eun-A; Sanders, Kenton M et al. (2018) SPORTS1.0: A Tool for Annotating and Profiling Non-coding RNAs Optimized for rRNA- and tRNA-derived Small RNAs. Genomics Proteomics Bioinformatics 16:144-151
Drumm, Bernard T; Sung, Tae S; Zheng, Haifeng et al. (2018) The effects of mitochondrial inhibitors on Ca2+ signalling and electrical conductances required for pacemaking in interstitial cells of Cajal in the mouse small intestine. Cell Calcium 72:1-17
Baker, Salah A; Drumm, Bernard T; Skowronek, Karolina E et al. (2018) Excitatory Neuronal Responses of Ca2+ Transients in Interstitial Cells of Cajal in the Small Intestine. eNeuro 5:
Drumm, Bernard T; Hennig, Grant W; Battersby, Matthew J et al. (2017) Clustering of Ca2+ transients in interstitial cells of Cajal defines slow wave duration. J Gen Physiol 149:703-725
Smith, Terence Keith; Koh, Sang Don (2017) A model of the enteric neural circuitry underlying the generation of rhythmic motor patterns in the colon: the role of serotonin. Am J Physiol Gastrointest Liver Physiol 312:G1-G14
Beckett, Elizabeth A H; Sanders, Kenton M; Ward, Sean M (2017) Inhibitory responses mediated by vagal nerve stimulation are diminished in stomachs of mice with reduced intramuscular interstitial cells of Cajal. Sci Rep 7:44759
Durnin, Leonie; Lees, Andrea; Manzoor, Sheerien et al. (2017) Loss of nitric oxide-mediated inhibition of purine neurotransmitter release in the colon in the absence of interstitial cells of Cajal. Am J Physiol Gastrointest Liver Physiol 313:G419-G433
Cobine, C A; Hannah, E E; Zhu, M H et al. (2017) ANO1 in intramuscular interstitial cells of Cajal plays a key role in the generation of slow waves and tone in the internal anal sphincter. J Physiol 595:2021-2041
Lee, Moon Young; Park, Chanjae; Ha, Se Eun et al. (2017) Serum response factor regulates smooth muscle contractility via myotonic dystrophy protein kinases and L-type calcium channels. PLoS One 12:e0171262

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