Our former work demonstrated that our impeller pump could support the circulation of experimental animals for several months without harm to blood elements or organ function. The termination of the experiments was mostly related to wear of the mechanical bearing and thrombosis along the bearing. To solve the bearing problem, we investigated a magnetic bearing in our lab, which resulted in some new problems, such as complicated design and control, considerable energy consumption, and lesser reliability. Progress in developing an impeller pump for long-term application has recently been achieved. Instead of using a sliding bearing system, we devised a rolling bearing system. Its service life is more than 10 years because of a wearproof roller made of ultra high molecular weight polythene. To avoid thrombus formation, we introduced a special purge system to the bearing, allowing the saline with heparin to be infused through the bearing into the pump. The bearing, therefore, keeps working in the saline, and no thrombus will be formed. Animal experiments demonstrated that a 30 ml fluid infusion per hour is enough to prevent thrombus formation. With these improvements, the impeller pump has continuously run for 8 months, and no bearing wear can be measured. The device, weighing 150 g, is fully implantable, consumes approximately 9.6 watts, and delivers a 9L/min blood flow against a 120 mm Hg mean pressure and reaches a highest total efficiency of 24.7% for the motor (including the controller) and pump. The system can produce both pulsatile and nonpulsatile flow according to requirements. 相似文献
Background: Despite years of research, the treatment of acute kidney injury (AKI) remains a significant challenge. Animal studies presented causal links between elevated regulatory T cell (Treg) response and better prognosis in AKI. Previous studies in mice and humans showed that TIM-3+ Treg cells were more potent than TIM-3- Treg cells. In this study, we investigated the role of TIM-3 in Treg in AKI patients.
Methods: Peripheral blood from AKI patients and healthy controls were gathered, and TIM-3+ Treg subset was examined.
Results: Compared to healthy controls, the AKI patients presented a significant upregulation in the frequency of circulating CD4+CD25+ T cells; however, the majority of this increase was from the CD4+CD25+TIM-3- subset, and the frequency of CD4+CD25+TIM-3+ T cells was downregulated in AKI patients. In both healthy controls and AKI patients, the CD4+CD25+TIM-3+ T cells expressed higher levels of Foxp3, and were more potent at expressing LFA-1, LAG-3, CTLA-4, IL-10 and TGF-β. In addition, the CD4+CD25+TIM-3+ T cells from both healthy controls and AKI patients presented higher capacity to suppress CD4+CD25- T cell proliferation than the CD4+CD25+TIM-3- T cells. Interestingly, the total CD4+CD25+ T cells from AKI patients presented significantly lower inhibitory capacity than those from healthy controls, indicating that the low frequency of CD4+CD25+TIM-3+ T cells was restricting the efficacy of the Treg responses in AKI patients.
Conclusions: We demonstrated that TIM-3 downregulation impaired the function of Treg cells in AKI. The therapeutic potential of CD4+CD25+TIM-3+ T cells in AKI should be investigated in future studies. 相似文献