This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The primary hypothesis of this protocol is: CP is a complex syndrome that is initiated by acute injury to the pancreas with a sustained or recurrent inflammatory response (Sentinel Acute Pancreatitis Event - SAPE Model hypothesis [1]). The secondary hypotheses: (1) RAP is a precursor of CP and that complex genetic, environmental and metabolic interactions determine the susceptibility to, and progression of CP. (2) Complications of CP, including inflammatory patterns and fibrosis, pain patterns and severity, calcifications, diabetes mellitus and malignancy represent abnormal responses of the immune system, vascular system, nervous system, endocrine system, and DNA repair systems rather than post-injury healing and regeneration. (3) Multiple pathways converge on the effector cell of pathology (e.g. the pancreatic stellate cell which is mediator of fibrosis) and that different combinations of pathologic pathways are responsible for driving undesirable outcomes in different people. (4) Statistical and mathematical modes can be constructed that incorporate knowledge of biology, all major risk factors, all major disease states and pathway-specific biomarkers and surrogate endpoints to accurately predict a variety of outcomes and scenarios in individual patients (personalized medicine). The goal of the NAPS2 program is to provide new insight into disease subtypes, risks, etiology, progression, complications, and outcomes, and to develop new predictive tools that will be useful in designing preventative approaches and effective treatments.
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