FasL^＋组织工程化猪软骨细胞的同种异体移植

目的:探讨表达FasL的猪组织工程化软骨细胞在同种异体内的生长状况和免疫排斥反应。方法:实验于2002-09/2004-03在上海交通大学医学院,上海市免疫学研究所进行。①分离制备猪软骨细胞。②制备FasL 软骨细胞,构建重组pGCEN-FasL反转录病毒载体,转染PA317细胞。经G418筛选获得分泌pGCEN-FasL病毒颗粒的PA317细胞克隆,选择高滴度的病毒液,感染猪软骨细胞。再经过G418筛选获得FasL 的软骨细胞克隆,扩增培养。③FACS检测FasL的表达,应用JAM试验测定FasL 的软骨细胞诱导Fas 的Jurkat细胞及活化的T细胞的凋亡率。同时制备转染pGCEN反转录病毒空载体的软骨细胞为对照。④取FasL 的软骨细胞与可注射性生物材料PluronicF127混合,注射于同种异体猪的腹壁皮下。在第4,5周取材,通过组织病理和免疫组织化学等方法,检测软骨细胞生长和免疫排斥反应。结果:①经转染的软骨细胞表面FasL的表达率为57%。②FasL 的软骨细胞具有明显诱导Fas 细胞和活化的同种异体T细胞的凋亡,最大的凋亡率分别为53.41%,30.38%(效/靶=10∶1),对照组分别为32.27%,13.16%(效/靶=10∶1)。③组织工程化猪软骨结节的结构与正常软骨组织基本一致,可见清晰的软骨凹陷和软骨膜,仅细胞排列较正常软骨略显混乱、不均匀现象。④免疫组织化学染色显示FasL 的组织工程化猪软骨结节的Ⅱ型胶原蛋白分布均匀,形状清楚,与正常软骨比较基本一致。⑤第5周的软骨细胞表面的FasL分子表达明显,周围的炎性细胞浸润相对较少。而对照组的软骨细胞周围可见到大量浸润的炎性细胞。结论:成功构建FasL 软骨细胞并有效表达,抑制免疫排斥反应,为建立同种异体软骨细胞移植的免疫耐受提供了实验依据。     

Snapping tendon syndrome: hip tenography with fluoroscopic monitoring

The snapping tendon syndrome may be caused by abnormalities of the fascia lata, gluteus maximus muscle, or less commonly, the iliopsoas tendon. One case is reported in which fluoroscopic monitoring after computed tomography-guided injection of contrast material confirmed the diagnosis of snapping iliopsoas tendon syndrome.     

Diagnosis of sustainable collaboration in health promotion – a case study

Background  

Collaborations are important to health promotion in addressing multi-party problems. Interest in collaborative processes in health promotion is rising, but still lacks monitoring instruments. The authors developed the DIagnosis of Sustainable Collaboration (DISC) model to enable comprehensive monitoring of public health collaboratives. The model focuses on opportunities and impediments for collaborative change, based on evidence from interorganizational collaboration, organizational behavior and planned organizational change. To illustrate and assess the DISC-model, the 2003/2004 application of the model to the Dutch whole-school health promotion collaboration is described.     

COMPLIANCE WITH PRESCRIBED MEDICINES IN GENERAL MEDICAL AND SURGICAL WARDS

SUMMARY A total of 6833 doses of medication were prescribed to 753 hospital inpatients in general wards over a 24-hour period (excluding medicines prescribed on an as-required basis and medicines prescribed for the first time during the 24-hour period). Of these, 574 (8.4%) doses were omitted, representing at least one omitted dose in 242 (32.1%) patients. Many of the omitted doses were of symptomatic treatments and in 43% of instances omission was deemed, retrospectively, to have been beneficial. Some omissions, however, were of a potentially life-threatening nature. The most common reasons for omission were that the patient refused the drug or that the nurse thought the drug unnecessary, the patient was on ‘nil by mouth’ or was too ill or unable to take the medicine. Thus, omission of prescribed medicines in general wards is common, often of little consequence or even beneficial, but of a potentially serious nature.     

β-环糊精流动相和手性配位交换HPLC法分离药物对映体

目的:为生物样品手性药物对照体的分离测定建立手性流动相添加剂HPLC,方法:以β-环糊精和手性配位交换剂为流动相添加剂,分离测定了生物样品中羟基苯妥英、美芬妥英、叔丁喘安、氯噻酮、氧氟沙星等5种手性药物对映体.结果:测得结果各对映体之间均能得到较好的分离.以β-环糊精为流动相添加剂法测得4种手性药物对映体的分离度(R)在1.10～1.86之间,各对映体的理论板数(n)在1642～2022之间.以手性配位交换法测得氧氟沙星两对映体的R为2.10,n为2560和 2600.并于制备柱上分离获得两对映体的纯品.结论:本法无需特殊设备,可在常规高效液相仪上进行手性药物的分离测定,操作简便、手性添加剂的种类多,适用范围广、便于推广     

Cellular regulation in friend virus induced erythroleukemia. Studies with anemic mice of genotype SI/SI(d)

Genetically anemic SI/SI(d) mice have been shown previously to have a defective hematopoietic environment which prevents extensive erythroid differentiation of normal hematopoietic stem cells and also confers resistance to the erythroleukemia-inducing virus, Friend spleen focus-forming virus (SFFV). In this study, we show that the relative resistance of SI/SI(d) mice to transformation by SFFV is not due to the inability of SFFV to replicate, nor is it because SFFV cannot transform erythroid cells, in the spleens of these mice. Injection of syngeneic +/+ mouse spleen cells, previously infected in vivo with SFFV, into secondary SI/SI(d) recipients resulted in marked splenic enlargement, and the appearance of large numbers of erythropoietin (Epo)-independent erythroid colonies in plasma clot culture. The cellular proliferation observed in these SI/SI(d) secondary recipients appeared to be due to infection and transformation of host SI/SI(d) cells rather than the growth of possible tumor colony-forming units (TCFU) present in the infected +/+ spleens, because preirradiation of the SI/SI(d) recipients abolished the splenomegaly and appearance of Epo- independent erythroid colonies. Furthermore, prior irradiation (1,200 rads) of donor spleen cells from SFFV-infected +/+ mice only slightly reduced spleen focus formation in unirradiated SI/SI(d) recipients. The conclusion that SI/SI(d) target cells could be infected and transformed by SFFV was confirmed directly by injecting a high titered preparation of SFFV into SI/SI(d) mice. SI/SI(d) mice were not absolutely resistant to infection or transformation by SFFV. Nevertheless, cells from the spleens of SFFV-infected mice were unable to form tumor colonies (TCFU) in irradiated SI/SI(d) recipients, suggesting that TCFU are either present at an undetectably low frequency in these spleens, or that they are still subject to the regulatory influences of the Steel locus.