NEW ONSET OF TYPE 1 DIABETES MYCOPHENOLATE MOFETIL-DACLIZUMAB

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。 新发的1型糖尿病霉酚酸酯？？Daclizumab临床试验 (TN-02号议定书) 通过免疫抑制保存胰腺产生的胰岛素-1研究版：2007年5月30日 印尼盾11528 版本2.0 由国家糖尿病和消化及肾脏疾病研究所、NIDDK、国家过敏和传染病研究所、NIAID、国家儿童健康和人类发展研究所、国家研究资源中心、国际青少年糖尿病研究基金会以及美国糖尿病协会赞助。 过去10？20年来发展的大量证据表明，人类1型糖尿病是一种慢性、缓慢进展的自身免疫性疾病。这项研究的目的是确定免疫干预策略，以防止从1型糖尿病发病时起β细胞破坏的进展。至少一些β细胞的持续存在应该会改善长期的糖尿病护理，不仅可以预防疾病本身的并发症，还可以预防低血糖，这是其管理的结果。其目的是阻止新糖尿病患者的β细胞破坏，因为一旦自身免疫过程进展到完全或接近完全破坏β细胞，免疫调节可能不会很好地发挥作用。 长期糖尿病的并发症是众所周知的，目前糖尿病及其并发症的护理费用每年超过1000亿美元。糖尿病控制和并发症试验和其他研究表明，改善代谢控制可以减少糖尿病的长期并发症[6]。因此，能够恢复正常胰岛功能和维持胰岛素产生的干预措施将显著改善糖尿病代谢控制的预后，从而减少长期并发症。

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. NEW ONSET OF TYPE 1 DIABETES MYCOPHENOLATE MOFETIL ¿?? DACLIZUMAB CLINICAL TRIAL (Protocol TN-02) Preservation of Pancreatic Production of Insulin through Immunosuppression - 1 Study EDITION: May 30, 2007 IND 11528 Version 2.0 Sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases; NIDDK;, the National Institute of Allergy and Infectious Diseases; NIAID;, the National Institute of Child Health and Human Development , the National Center for Research Resources, the Juvenile Diabetes Research Foundation International;, and the American Diabetes Association;. The great body of evidence developed over the last 10 ¿?? 20 years suggests that type 1 diabetes in humans is a chronic, slowly progressive autoimmune disease. The objective of this study is to identify immune intervention strategies that will prevent the progression of beta cell destruction from the time of onset of type 1 diabetes. The persistence of at least some beta cells should improve long-term diabetes care and prevent not only complications of the disease itself but also hypoglycemia, which is a consequence of its management. The aim is to arrest beta cell destruction in newly diabetic subjects because immune modulation may not work well alone once the autoimmune process has progressed to complete or near complete destruction of beta cells. The complications of long-term diabetes are well known, and the costs of caring for diabetes and its complications are currently greater than $100 billion a year. The Diabetes Control and Complications Trial and other studies have demonstrated that improved metabolic control can reduce the long-term complications of diabetes [6]. Thus, an intervention, which could restore normal islet function and maintain production of insulin would significantly improve the prognosis for metabolic control of diabetes and thus reduce long-term complications.