| 2 | Delayed treatment of secondary degeneration following acute optic nerve transection using a combination of ion channel inhibitors显示文摘Studies have shown that a combined application of several ion channel inhibitors immediately after central nervous system injury can inhibit secondary degeneration. However, for clinical use, it is necessary to determine how long after injury the combined treatment of several ion channel inhibitors can be delayed and efficacy maintained. In this study, we delivered Ca^(2+) entry-inhibiting P2X7 receptor antagonist oxidized-ATP and AMPA receptor antagonist YM872 to the optic nerve injury site via an iPRECIO~@ pump immediately, 6 hours, 24 hours and 7 days after partial optic nerve transection surgery. In addition, all of the ion channel inhibitor treated rats were administered with calcium channel antagonist lomerizine hydrochloride. It is important to note that as a result of implantation of the particular pumps required for programmable delivery of therapeutics directly to the injury site, seromas occurred in a significant proportion of animals, indicating infection around the pumps in these animals. Improvements in visual function were observed only when treatment was delayed by 6 hours; phosphorylated Tau was reduced when treatment was delayed by 24 hours or 7 days. Improvements in structure of node/paranode of Ranvier and reductions in oxidative stress indicators were also only observed when treatment was delayed for 6 hours, 24 hours, or 7 days. Benefits of ion channel inhibitors were only observed with time-delayed treatment, suggesting that delayed therapy of Ca^(2+) ion channel inhibitors produces better neuroprotective effects on secondary degeneration, at least in the presence of seromas. | Nathanael J.Yates Marcus K.Giacci Ryan L. O'Hare Doig Wissam Chiha Bethany E. Ashworth Jade Kenna Carole A. Bartlett Melinda Fitzgerald | 2017 | Neural Regeneration Research2017，12，2： | 0 |
| 3 | 经十二指肠EUS确定原发性硬化性胆管炎中肝外胆管树管壁增厚显示文摘Background: Diagnosing primary sclerosing cholangitis (PSC) is problematic and requires meeting a burden of proof through clinical, biochemical, radiologic, and histological features. Endoscopic ultrasound yields detailed images of the extrahepatic biliary tree, but its value in contributing to the diagnosis of this condition is unknown. Objectives: To determine the potential for transduodenal EUS to detect common bile duct wall thickening in PSC.Design: A prospective, controlled study with retrospective, blinded data analysis. Setting: Single tertiary referral center for inflammatory bowel disease and EUS. Patients: Four groups of patients were assessed with radial endosonography: PSC (n = 9); inflammatory bowel disease (IBD) with abnormal liver blood tests (n = 21); choledocholithiasis (n = 15); and normal controls (n = 50). Measurements were made of the common bile duct diameter and wall thickness. Interventions: Transduodenal radial EUS of the biliary tree. Main Outcome Measurements: Common bile duct diameter and wall thickness. Results: The mean diameter (SD) of the common bile duct for the PSC, IBD, choledocholithiasis, and normal control groups measured 8.9 mm (2.8), 5.4 mm (1.7), 7.2 mm (2.2), and 5.0 mm (1.9), respectively (PSC and chole-docholithiasis groups compared to the IBD group, P < .05 for a single test of hypothesis, but correction for the multiple testing of data removed this significance; normal control group P < .005). Mean ductal wall thickness (SD) was 2.5 mm (0.8) for the PSC group, 0.7 mm (0.4) for the IBD group, 0.8 mm (0.4) for the choledocholithiasis group, and 0.8 mm (0.4) for the normal control group, respectively (PSC group compared to the other 3 groups, P < .005). Limitations: Assessment of intrahepatic PSC is problematic. Conclusion: Thickening ( >1.5 mm) of the common bile duct wall is seen in patients with PSC but not in those with aPPArently uncomplicated IBD or choledocholithiasis. The results of this study suggest that standard endosonography contributes to the imaging and potentially to the diagnosis of PSC. | Mesenas S. Vu C. Doig L. Meenan J. 陈瑜(译) 郑世成(校) | 2006 | 世界核心医学期刊文摘(胃肠病学分册)2006，2，8： | 0 |
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