Quality assessment and assurance in diagnostic imaging. Theoretical and practical considerations and a quality audit of the excretory urogram

Concepts necessary to an understanding of the basics of quality assurance audits are presented. Included are specific examples that bridged theory and practice by applying the protocol to a real-life diagnostic imaging situation. This method meets the present requirements of the Joint Commission of the Accrediation of Hospitals.     

Colon perforation following percutaneous nephrostomy and renal calculus removal

Two patients had colonic perforation as a result of percutaneous nephrostomy placement followed by track dilatation and renal calculus removal. We present the technical aspects of nephrostomy placement and stone removal, as well as the clinical diagnosis and management of these cases. Both patients recovered well with conservative therapy and required no surgical intervention. This report reviews the anatomic considerations for percutaneous nephrostomy in patients undergoing renal stone removal.     

虚拟现实技术在运动康复中的应用

目的:介绍虚拟现实技术在运动功能障碍的康复性训练领域的应用和新发展,讨论虚拟现实技术应用于运动康复的优势和前景。资料来源:应用计算机检索外文期刊PsycINFO和PubMed数据库1996/2006与虚拟现实技术在康复训练中应用相关的文章,检索语种为“English”,检索词为“motor rehabilitation,virtual reality”。检索中文期刊CNKI数据库1996/2006相关的文献,检索语种为中文,检索词为“康复,虚拟现实”。资料选择:根据摘要和关键词对资料进行初选,选择全面介绍虚拟现实技术的文章,以及近几年将虚拟现实技术应用于空间感知障碍和运动功能受损患者康复训练的实验研究报告。资料提炼:在上述3个数据库中分别检索到相关英文文献121篇,以及中文文献21篇,按上述标准纳入18篇,再继续搜索已有文献引用和被引用的参考文献,最后得到相关的中英文文献30篇。资料综合:30篇文献中,4篇文章详细介绍了虚拟现实技术在运动康复领域的应用,26篇实验报告了应用虚拟现实对受损的运动功能进行康复性训练的成效。按照运动康复的种类将研究报告分为4类:平衡和姿态训练、行走训练、上下肢康复训练和日常生活技能训练。通过模仿练习,感知运动受损的患者可以在虚拟环境中完成针对性训练任务,学会运动技能。在虚拟环境中习得的运动技能可以迁移到现实世界的真实任务中。结论:与传统康复训练方法相比,虚拟现实具有更安全、更有趣、针对性强、康复速度快、疗效好等优势。作为一种有效的运动康复技术手段,虚拟现实技术有很好的发展前景。     

Platelet adhesion and thrombus formation on subendothelium in platelets deficient in glycoproteins IIb-IIIa, Ib, and storage granules

Patients whose platelets are deficient in glycoprotein (GP) Ib, IIb- IIIa (thrombasthenia), or granule substances (storage pool deficiency, SPD) were studied to define further the properties of platelets that mediate platelet adhesion and thrombus formation on subendothelium. Both nonanticoagulated and citrated blood were exposed to everted, de- endothelialized rabbit vessel segments under controlled flow conditions and shear rates varying from 650 to 3,300 sec-1. Morphometry was used to measure platelet thrombus dimensions and the percentage of the subendothelial surface covered with contact (C) or spread (S) platelets. Adhesion was defined as C + S. The results in SPD demonstrated (1) reduced thrombus dimensions in delta-SPD (pure dense granule deficiency) in proportion to the magnitude of the dense granule defect; (2) an even greater reduction in thrombus dimensions in patients with combined deficiencies of alpha and dense granules (alpha delta-SPD); and (3) impaired platelet adhesion at several conditions in alpha delta-SPD and, in delta-SPD, a hematocrit-dependent impairment of adhesion in citrated blood at 2,600 sec-1. In thrombasthenia, platelets were present as a monolayer on the subendothelial surface in both nonanticoagulated and citrated blood, indicating an absolute requirement for GPIIb-IIIa in promoting platelet-platelet interaction at all shear rates and perfusion times. Two types of abnormalities in platelet-vessel wall interactions were observed. In nonanticoagulated blood, the percentage of platelets in the C phase was consistently increased at all shear rates, but C + S values were normal. These observations indicate that platelets deficient in GPIIb-IIIa do not spread normally on the subendothelial surface exposed to nonanticoagulated blood. With citrated blood, the C + S value in thrombasthenia was reduced at both 800 and 2,600 sec-1, as in von Willebrand's disease, and a similar degree of reduction (about 50%) was observed in normal blood treated with a monoclonal antibody to GPIIb- IIIa. The findings, together with theoretical considerations, are consistent with an hypothesis that GPIIb-IIIa mediates the spreading of platelets on subendothelium following the initial attachment through GPIb and that GPIIb-IIIa may be considered an adhesion site on the platelet membrane. Abnormalities of GPIIb-IIIa may, depending on the conditions of study, result in either increased values of C platelets or decreased values of C + S. The results of the study further suggest that a complex interaction of platelet granule factors and membrane GP mediate platelet adhesion and thrombus formation.     

Fanconi's anemia treated by allogeneic marrow transplantation

Eight patients with Fanconi's anemia were given cyclophosphamide alone (seven patients) or combined with procarbazine and antithymocyte globulin (one patient) followed by marrow grafts from HLA-identical siblings. All patients had engraftment. Seven developed acute and three chronic graft-versus-host disease (GVHD). Three patients died with GVHD and infectious complications (days 19, 56, and 82) and one with an intracerebral hemorrhage (day 540). Four patients are surviving 647- 3435 days after grafting, two are well, and two have chronic GVHD that is improving. These results show that Fanconi's anemia can be treated successfully by allogeneic marrow transplantation.     

Prednisone can protect against exercise-induced muscle damage

In an experimental animal exercise model we tested whether daily administration of prednisone prevents the development of mechanically induced muscle fibre damage. Six-week-old rats were treated with different doses of prednisone ranging from 1 to 50 mg/kg body weight per day or with placebo, for 8 days. On day 6 of treatment the rats were forced to run for 2 h on a level treadmill. Two days after exercise morphological damage in the soleus muscles was quantified using light microscopy and a semi-automatic image analysis system. Creatine kinase (CK) activity was measured before exercise (day 5) and directly after exercise (day 6). The expression of dystrophin in a placebo group and in a group that received 5 mg prednisone/kg body weight per day with and without performing exercise was studied with Western blotting. The effect of prednisone on fibre type distribution was determined with an antibody against fast myosin and the effect of prednisone on the proliferative activity of muscle satellite cells was studied using bromodeoxyuridine (BrdU) immunohistochemistry. Exercise-induced muscle fibre damage varied in a dose-dependent way. In the placebo group the mean (SEM) damaged muscle fibre area was 4% (1%). The groups that received low doses of prednisone, 1 or 2.5 mg/kg per day, showed a similar level of muscle damage. However, with 5 mg prednisone/kg per day the amount of muscle fibre damage [mean (SEM)] was significantly reduced to 1.4% (0.5%) (P 0.05, Student'st-test). High doses of prednisone had no protective effect. Directly after exercise the CK activity was increased two-fold, except in the group that received 50 mg prednisone/kg body weight per day. No changes in the amount of dystrophin were found after densitometric analysis of the Western blots. Prednisone did not affect the fibre distribution or the labelling index of satellite cells. We conclude that prednisone, given in an appropriate dose, protects muscle fibres against the development of mechanically induced damage, possibly by stabilizing the muscle fibre membranes. This action may explain the beneficial effect of prednisone observed in Duchenne muscular dystrophy patients.