镍钛记忆合金锁骨钩环抱器治疗新鲜重度肩锁关节脱位

目的 评估镍钛记忆合金锁骨钩环抱器治疗新鲜重度肩锁关节脱位的临床疗效。方法 选择16例新鲜重度肩锁关节脱位患者，其中3例合并锁骨远端骨折，应用镍钛记忆合金锁骨钩环抱器治疗并进行临床疗效观察。随访6～12个月，平均7.6个月。结果 所有患者肩关节肌肉无萎缩，外观正常，肩关节活动范围正常，x线片示无再脱位征象。采用Karlsson术后疗效分级：A级15例，B级1例。结论 镍钛记忆合金锁骨钩环抱器治疗新鲜重度肩锁关节脱位创伤小，简便易行，疗效好，对合并锁骨远端骨折病人更具有独特优点，具有临床推广应用价值。     

肩锁钩板治疗不稳定性锁骨外侧段骨折的临床研究

目的：比较肩锁钩板和传统克氏针内固定治疗不稳定性锁骨外侧段骨折的疗效。方法：54例不稳定性锁骨外侧段骨折的患者接受了手术治疗，内固定分别是锁骨钩板或克氏针，根据国外的锁骨外侧段骨折肩部功能评价标准进行6－12个月的术后随访，随访结果运用统计学方法进行分析处理，结果：克氏针内固定组的手术优良率为77．3％，并发症发生率为27．3％，骨折愈合率为81．8％；锁骨钩板内固定组的手术优良率为100％，并发症发生率为3．1％，骨折愈合率100％。两组数据统计学差异有显著性，结论：在不稳定性锁骨外侧段骨折的手术治疗中，锁骨钩板较传统克氏针内固定有较高的手术优良率和骨折愈合率，且并发症的发生率较低，因此，它是一种疗效满意的内固定方法。     

青年性腰椎弓根崩裂直接修复后TSRH钩钉系统固定12例初步报告

[目的]评价TSRH钩钉系统对青年患者腰椎弓崩裂直接修复后固定的临床疗效。[方法]自2001年7月~2003年10月,对12例男性单纯腰椎弓崩裂患者(16~31周岁)行腰椎弓崩裂自体骨直接修复峡部裂后TSRH椎板钩、椎弓根钉固定术。术后随访,根据术后X线、CT结果评价修复效果,并根据MacNab's标准进行临床评价。[结果]经过6~19个月随访,所有患者腰椎弓崩裂影像学全部融合;临床下腰痛显著缓解,按MacNab's标准,优8例,良3例,一般1例;无手术及内固定相关并发症发生。[结论]直接修复后TSRH钩钉系统固定治疗青年性腰椎弓崩裂能充分保留腰椎运动节段,在减少融合节段的同时能有效恢复腰椎稳定,操作简便、安全,固定可靠,是一种合乎逻辑的治疗青年性腰椎弓崩裂方法。     

AO肩锁钢板钩治疗重型肩锁关节脱位

目的评估AO肩锁钢板钩治疗重型肩锁关节脱位的手术疗效.方法回顾性分析两年来27例手术病人的手术治疗和疗效.结果手术方法符合生理结构,手术时间平均30分钟,内固定牢靠.根据Murley和Constant[1]评分,优良率94%.结论 AO肩锁钢板钩治疗重型肩锁关节脱位,手术方法简单,疗效可靠,允许病人术后早期功能锻炼.     

Interleukin-1 beta gene polymorphism related with allergic pathogenesis in Iris constitution

Iridological constitution has a strong familial aggregation and is implicated in heredity. The aetiology of inflammatory bowel disease is still unknown. However, from genetic epidemiological studies there is considerable evidence that genetic factors are associated with both Crohn's disease and ulcerative colitis. We investigated the relationships between Iridological constitution and interleukin 1 beta (IL-1β) gene polymorphism. IL-1β is a major proinflammatiry cytokine, and the polymorphisms of this gene have been shown to be of importance in a number of diseases. Especially, IL-1 has been suspected of involvement in allergic pathogenesis. Also, IL-1β genotype is one of the genetic markers of gastric cancer. Therefore, we classified 166 individuals according to Iris constitution, and determined IL-1β genotype. The frequencies of Iris constitutions as follows: neurogenic type, 41 (24.7%); abdominal connective tissue weakness type, 53 (31.9%); cardio-renal connective tissue weakness type, 50 (30.1%); the others type, 22 (13.3%). Especially, the frequency of abdominal connective tissue weakness type was higher in C/T genotype than in the remaining constitutions although the statistical power was very weak. Furthermore, we first attempted to explore possible involvement of the IL-1β polymorphism and the Iris constitution.     

Iris (Lisch) nodules in neurofibromatosis

A group of 30 patients ranging from 4 to 56 years of age with the peripheral form of neurofibromatosis were evaluated for the presence of iris (Lisch) nodules. These nodules were observed in 73% of our cases and their presence was directly related to the severity of the skin manifestations of the disease. It is concluded that Lisch nodules are pathognomonic for neurofibromatosis and thus, their presence should be looked for in all suspected cases.     

Chlorhexidine-induced degeneration of adrenergic nerves

Summary Possible toxic effects of chlorhexidine (CHX) on the sympathetic adrenergic ground plexus were studied in whole mounts of albino rat irides using Falck-Hillarp fluorescence histochemistry. CHX dissolved in an isotone, buffered sodium-acetate solution or in 70% alcohol was injected into the anterior chamber of eye. CHX caused a marked and dose-dependent degeneration of adrenergic nerves. Two days after the lowest dose, 0,25 g (5 l of a 0.05% CHX solution), approximately 30% of the nerves had disappeared. Almost complete degeneration was observed after the same time with higher doses (2.5 g, 5.0 g, and 7.5 g corresponding to 0.5, 1.0, and 1.5% CHX respectively). Two weeks after the lowest dose, the nerves had regenerated almost completely. With the highest dose used, only some 40% of the normal adrenergic nerve plexus had reformed after 51 days. Alcohol as a solvent did not have an additive effect on the neurotoxic action caused by CHX. The results demonstrate yet another aspect of chlorhexidine neurotoxicity, degeneration of peripheral adrenergic nerve terminals. This suggests that neurotoxic actions on thin unmyelinated fiber systems should be looked for also in the central nervous system (CNS).Supported by the Swedisch Council for Planning and Coordination of Research (Project: Chemical Hazards in the Environment), The Swedish Medical Research Council (14X-03185; 14P-5867; 04P-6889), Magnus Bergvalls Stiftelse, and Karolinska Institute Fonder