Switch From Twice-daily Tacrolimus to Once-daily,Prolonged-release Tacrolimus in Kidney Transplantation: Long-term Outcome

Background

One daily dose of tacrolimus (QDT) improves adherence in kidney transplant (KT) recipients. A switch from twice-daily tacrolimus (BDT) to QDT showed similar efficacy and safety.

电视胸腔镜胸腺手术的围术期处理

目的：探讨电视胸腔镜胸腺手术的围术期处理方法。方法：2000年1月至2002年8月我院应用电视胸腔镜手术(VATS)进行胸腺手术共lO例。胸腺瘤6例，胸腺囊肿2例，胸腺增生1例，恶性胸腺瘤1例。重症肌无力3例，按Ossermen分型Ⅰ型l例，ⅡA型2例。结果：9例于胸腔镜下完成，l例中转开胸完成，全组无并发症，无一死亡，均治愈出院。结论：适当选择病例、合理的围术期处理是顺利完成胸腔镜胸腺手术的保证。     

Monoamine oxidase-B inhibition: a comparison of in vivo and ex vivo measures of reversible effects

Summary A behavioural test involving potentiation of the effects of an acute injection of -phenylethylamine (10 mg kg^–1 i.p.) was used to assess the time-course of type-B MAO inhibition after administration of (–)deprenyl (5 mg kg^–1 i.p.) and of MD 240928 (20 mg kg^–1 i.p.) respectively. Potentiation of the effects of -phenylethylamine was observed 1 h after injection of (–)deprenyl or MD 240928. This effect was still evident 120 h after administration of (–)deprenyl but not 24 h after administration of MD 240928. Comparisons of ex vivo estimates of MAO activity yielded a corresponding time-course for the recovery of this enzyme. The extent of MAO inhibition required for potentiation of the effects of -phenylethylamine was inferred from a comparison of the behavioural test results and the ex vivo MAO activity observed after (–)deprenyl administration. These comparisons indicate a significant underestimation of MD 240928-induced MAO inhibition using ex vivo measures. This underestimation is interpreted as evidence fordilution effects in the ex vivo assay of MAO inhibition. The potentiation of effects of -phenylethylamine under the present conditions is proposed as a useful and simple test for effects of reversible type-B MAO inhibitors.     

Transient aphasia with lithium toxicity

A case of transient aphasia in a 48-year-old woman is described. The aphasia occurred when progressive renal insufficiency led to accumulation of lithium to toxic levels, and was associated with well-known clinical findings of lithium toxicity.