Browsing by Subject "pancreas"
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Item Pancreatic mitochondrial complex I exhibits aberrant hyperactivity in diabetes(Elsevier Inc., 2017-07-19) Wu, Jinzi; Luo, Xiaoting; Thangthaeng, Nopporn; Sumien, Nathalie; Chen, Zhenglan; Rutledge, Margaret A.; Jing, Siqun; Forster, Michael J.; Yan, Liang-JunIt is well established that NADH/NAD(+) redox balance is heavily perturbed in diabetes, and the NADH/NAD(+) redox imbalance is a major source of oxidative stress in diabetic tissues. In mitochondria, complex I is the only site for NADH oxidation and NAD(+) regeneration and is also a major site for production of mitochondrial reactive oxygen species (ROS). Yet how complex I responds to the NADH/NAD(+) redox imbalance and any potential consequences of such response in diabetic pancreas have not been investigated. We report here that pancreatic mitochondrial complex I showed aberrant hyperactivity in either type 1 or type 2 diabetes. Further studies focusing on streptozotocin (STZ)-induced diabetes indicate that complex I hyperactivity could be attenuated by metformin. Moreover, complex I hyperactivity was accompanied by increased activities of complexes II to IV, but not complex V, suggesting that overflow of NADH via complex I in diabetes could be diverted to ROS production. Indeed in diabetic pancreas, ROS production and oxidative stress increased and mitochondrial ATP production decreased, which can be attributed to impaired pancreatic mitochondrial membrane potential that is responsible for increased cell death. Additionally, cellular defense systems such as glucose 6-phosphate dehydrogenase, sirtuin 3, and NQO1 were found to be compromised in diabetic pancreas. Our findings point to the direction that complex I aberrant hyperactivity in pancreas could be a major source of oxidative stress and beta cell failure in diabetes. Therefore, inhibiting pancreatic complex I hyperactivity and attenuating its ROS production by various means in diabetes might serve as a promising approach for anti-diabetic therapies.Item Review of Blunt Pancreatic Trauma and Its Outcome(2007-12-01) Sanghvi, ChiragSanghvi, Chirag. Review of Blunt Pancreatic Trauma and Its Outcome. Master of Public Health (Biostatistics), December 2007, 37 pp., 4 tables, bibliography, 42 titles. Blunt pancreatic trauma (BPT) is an uncommon injury involving 1%-2% of blunt abdominal traumas but it can be associated with a high complication rate. Various studies have shown complication rate to range from 30%-64% following blunt pancreatic injury. With Institutional Review Board (IRB) approval a retrospective chart review study was performed for last 12 years. Chart review failed to support the hospital assigned diagnosis of BPT in 3 patients, leaving 37 cases for analysis. BPT had an overall mortality rate of 22%. In the patients surviving the injury, early surgical intervention (≤12 hours) had a complication rate of 31% versus 57% for delayed surgical intervention ([greater than] 12 hours). BPT has a high mortality rate but is usually secondary to other organs involved in the injury. Delayed surgical intervention has a higher complication rate compared to early intervention.