Bile duct stones: percutaneous transhepatic removal

Percutaneous transhepatic intervention for transduodenal removal of biliary stones was performed 38 times in 34 patients with obstructive jaundice, biliary colic, and cholangitis. The technique entailed the percutaneous transhepatic placement of a modified Dormia basket in the common duct with the flexible tip in the duodenum. The stones were passed into the duodenum and were crushed, or were crushed in the common duct and passed as fragments into the duodenum. In addition to the snare procedure, monooctanoin was used 18 times to dissolve remaining fragments of stone and sludge that could not be snared and passed into the duodenum. The average time for completion of the procedure was 10 days. There were no deaths from the procedure. The complication rate was 21%--probably no greater than would occur with surgery in a similar patient population. The procedure can be performed when endoscopic retrograde cholangiopancreatography and sphincterotomy with stone removal is technically impossible or refused, and in patients who have previously undergone choledochojejunostomy.     

Ongoing challenges in pediatric hospice care

Reports have begun to proliferate throughout the world which describe various models of pediatric hospice care. While encouraging, these reports identify universal obstacles that continue to compromise effective care. Challenges persist in areas of pain management, medical ethics, program administration, cost analysis, staff development and bereavement follow-up. Cooperative efforts are encouraged to address these issues.     

褪黑素对小鼠免疫性肝损伤的保护作用

目的观察褪黑素（MT）对小鼠免疫性肝损伤的影响。方法序贯注射短小棒状杆菌和脂多糖诱导小鼠免疫性肝损伤模型;在造模不同时间注射不同剂量MT;检测血浆转氨酶、肝脏雨二醛（MDA）和谷胱甘肽过氧化物酶（GSH-px）以及脾淋巴细胞增殖状况。结果造模期间用MT（0.1～10.0mg·kg-1）能显著降低血浆转氨酶和肝脏MDA水平（P＜0.05～0.01），使肝脏GSH-px活性部分恢复（P＜0.05），并能选择性抑制刀豆蛋白A诱导的脾淋巴细胞增殖。但造模后使用MT对免疫性肝损伤无明显影响。结论MT保护免疫性肝损伤作用与其抗氧化和免疫调节作用有关。     

The pathogenesis of diabetic retinopathy

Diabetic retinopathy remains a major cause of loss of vision. The Diabetes Control and Complications Trial (DCCT) has implicated hyperglycaemia as a probable major direct causative factor in the pathogenesis of diabetic retinopathy. There are several plausible mechanisms by which high glucose concentrations could lead to the functional and later structural changes characterising diabetic retinopathy. These include increased activity of the aldose reductase pathway, increase de novo synthesis of diacylglycerol from glucose, causing protein kinase C activation, increased non-enzymatic glycation and increased oxidative damage. The demonstration of the potential roles of these pathways and the subsequent effects of growth factors in enhancing angiogenesis provide potential new approaches to the prevention and treatment of diabetic retinopathy.