模拟航天超重状态下冲击过载致腹部脏器损伤的实验研究

目的 制作模拟航天超重状态下冲击过载致腹部脏器损伤的实验动物模型,探讨其损伤特点.方法 实验动物为ICR小鼠,利用离心机和脾中部横夹法造成模拟航天超重状态下冲击过载致腹部脏器损伤的实验动物模型,分时相测定血常规和组织病理学观察.结果 模型制作后,各时相/组实验动物的血常规中WBC、RBC、HGB、MCH、MCHC、PLT较正常组均有变化(P＜0.05);各时相/组实验动物的病理变化具有一定规律,其中病理变化以脾脏最为明显.结论 初步探讨了模拟航天超重状态下冲击过载致腹部脏器损伤后的损伤特点,总结致伤规律,可为进一步开展相关航天医学研究提供参考.     

Evaluation of the inferior vena cava by sonography and venography in children with renal and hepatic tumors

Ultrasonography was used to examine 81 children with intra-abdominal or retroperitoneal malignancies for tumor extension into the inferior vena cava (IVC). In seven of the 18 patients with Wilms tumors and three of the seven patients with hepatic tumors, the IVC ws sonographically abnormal. Venography was also performed in five patients with Wilms tumors. However, percutaneous transfemoral venacavography did not always allow differentiation between extrinsic compression and intracaval tumor. It is suggested that venacavography, when necessary, should be performed via the brachial vein route and that the catheter be advanced into the right atrium. If an injection in this chamber does not result in enough reflux into the retrohepatic IVC for adequate evaluation, the catheter should be advanced into the IVC and a second injection made. However, ultrasonography is the preferred modality for evaluation of the IVC in children because it is the most accurate method and is noninvasive. Real-time ultrasonography makes it possible to distinguish between tumor extension into the lumen of the IVC and extrinsic compression of the vessel.     

Plasminogen activator inhibitor-1 and diabetic nephropathy

SUMMARY:   Diabetic nephropathy is characterized by excessive accumulation of extracellular matrix (ECM) in the kidney. Decreased ECM degradation as well as increased ECM synthesis plays an important role in ECM remodeling that favours tissue fibrosis. Plasminogen activator (PA)/plasmin/PA inhibitor (PAI) system is involved in ECM degradation and PAI-1 plays a critical role in ECM remodeling in the kidney. Normal human kidneys do not express PAI-1 but PAI-1 is overexpressed in pathologic conditions associated with renal fibrosis including diabetic nephropathy. Reactive oxygen species mediate PAI-1 up-regulation in renal cells cultured under high glucose, hypoxia, and TGF-β1. Recent studies utilizing PAI-1 deficient mice suggest that PAI-1 induce ECM deposition in diabetic kidney through increased ECM synthesis by TGF-β1 up-regulation as well as through decreased ECM degradation by suppression of plasmin and MMP-2 activity.