THE NORTH AMERICAN PANCREATITIS STUDY

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 这一方案的基本假设是：CP是一种复杂的综合征，由胰腺急性损伤和持续或反复的炎症反应引起(前哨急性胰腺炎事件-SAPE模型假说[1])。 第二假设：(1)RAP是CP的前体，复杂的遗传、环境和代谢相互作用决定了CP的易感性和进展。(2)CP的并发症，包括炎症类型和纤维化、疼痛类型和严重程度、钙化、糖尿病和恶性肿瘤，是免疫系统、血管系统、神经系统、内分泌系统和DNA修复系统的异常反应，而不是损伤后的愈合和再生。(3)多条途径汇聚在病理效应细胞上(如作为纤维化介质的胰星状细胞)，不同的病理途径组合导致不同人的不良结局。(4)可以构建包含生物学知识、所有主要风险因素、所有主要疾病状态以及特定于路径的生物标记物和替代终点的统计和数学模型，以准确地预测个体患者的各种结果和情景(个性化医疗)。 NAPS2计划的目标是为疾病亚型、风险、病因、进展、并发症和结果提供新的见解，并开发新的预测工具，这些工具将有助于设计预防方法和有效的治疗方法。

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.