secretarial support, laboratory space, technical help, start-up funds and 80% protected time have been ensured for the candidate. The collaborative environment at the University of iowa and College of Medicine is particularly conducive towards the advancement of science and the nurturing of new investigators. Dr. Rory Fisher, PhD, Associate Professor, Department of Pharmacology, has extensive knowledge, experience, and expertise in the study of G-protein coupled receptors. His laboratory routinely performs the competitive bindingassays and signal transduction studies described in this protocol. Dr. Fisher is an enthusiastic teacher and will play an important collaborative role in this project. The candidate will receive training in molecular aspects of studies in receptor function and signal transduction in Dr. Fisher's laboratory. Dr. Christie Thomas, MD, Associate Professor of Nephrology, has assisted the candidate develop the ribonuclease protection assay for rat cholecystokinin-A receptor mRNA and will collaborate for future mRNA studies involved inthe project. Dr. David Elliott, MD, PhD, Associate Professor of Gastroenterology, is a member of Dr. Weinstock's laboratory team and will collaborate in investigations involving receptor function and regulation of inflammatory mediators. Clearly, full advantage is being taken of the rich collaborative resources available in the environment to enable the success of this research proposal and the training of the candidate. 5b) Institutional Commitment to Candidate's Research Career Development Dr. Carol Scott-Connor, MD, PhD, Head of the Department of Surgery, recruited the candidate for the principal purpose of building a basic science research laboratory. The candidate has been granted 80% protected time from the date of joining the faculty to pursue basic science research. The candidate was given top priority in terms of the provision of laboratory space, technical assistance, and financial resources required to begin his research immediately. The candidate has been assured of similar and continuing support in the future. The Department of Surgery and the University of Iowa College of Medicine have an unwavering commitment to the scientific training and development of the candidate. Evidence of the institutionalcommitment to the candidate's research career development is further documented in letters from Dr. Carol Scott-Conner, MD, PhD, Professor and Head of the Department of Surgery, and Dr. James W. Maher, MD, Director, Division of Gastrointestinal Surgery, University of Iowa College of Medicine, Iowa City. [] PHS 398/2590 (Rev. 05/01) Page__ 26 Continuation Format Page []

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08DK062805-05
Application #
7174243
Study Section
Diabetes, Endocrinology and Metabolic Diseases B Subcommittee (DDK)
Program Officer
Podskalny, Judith M,
Project Start
2003-01-15
Project End
2008-08-30
Budget Start
2006-12-01
Budget End
2008-08-30
Support Year
5
Fiscal Year
2007
Total Cost
$125,010
Indirect Cost
Name
University of Iowa
Department
Surgery
Type
Schools of Medicine
DUNS #
062761671
City
Iowa City
State
IA
Country
United States
Zip Code
52242
Samuel, Isaac; Tephly, Linda; Williard, Deborah E et al. (2008) Enteral exclusion increases MAP kinase activation and cytokine production in a model of gallstone pancreatitis. Pancreatology 8:6-14
Meyerholz, David K; Williard, Deborah E; Grittmann, Ana-Maria et al. (2008) Murine pancreatic duct ligation induces stress kinase activation, acute pancreatitis, and acute lung injury. Am J Surg 196:675-82
Samuel, Isaac (2008) Bile and pancreatic juice exclusion activates acinar stress kinases and exacerbates gallstone pancreatitis. Surgery 143:434-40
Meyerholz, David K; Samuel, Isaac (2007) Morphologic characterization of early ligation-induced acute pancreatitis in rats. Am J Surg 194:652-8
Samuel, Isaac; Yorek, Mark A; Zaheer, Asgar et al. (2006) Bile-pancreatic juice exclusion promotes Akt/NF-kappaB activation and chemokine production in ligation-induced acute pancreatitis. J Gastrointest Surg 10:950-9
Mattson, David L; Kunert, Mary Pat; Roman, Richard J et al. (2005) Substitution of chromosome 1 ameliorates L-NAME hypertension and renal disease in the fawn-hooded hypertensive rat. Am J Physiol Renal Physiol 288:F1015-22
Samuel, Isaac; Zaheer, Smita; Zaheer, Asgar (2005) Bile-pancreatic juice exclusion increases p38MAPK activation and TNF-alpha production in ligation-induced acute pancreatitis in rats. Pancreatology 5:20-6
Samuel, Isaac; Chaudhary, Ashok; Fisher, Rory A et al. (2005) Exacerbation of acute pancreatitis by combined cholinergic stimulation and duct obstruction. Am J Surg 190:721-4
Samuel, Isaac; Toriumi, Yasuo; Zaheer, Asgar et al. (2004) Mechanism of acute pancreatitis exacerbation by enteral bile-pancreatic juice exclusion. Pancreatology 4:527-32
Samuel, Isaac; Zaheer, Asgar; Zaheer, Smita et al. (2004) Bile-pancreatic juice exclusion increases cholinergic M3 and CCK-A receptor expression and interleukin-6 production in ligation-induced acute pancreatitis. Am J Surg 188:511-5

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