Micro-tubular cell development

The development of such SOFC is promoted by a Swiss consortium led by ETH Zurich [23] and in Germany, a new start-up company named eZelleron presented micro tubular SOFC [24] which can be scaled from 1/5 (nominal/peak load) W for battery chargers for mobile phones etc., to 25/125 W for laptop computers and leisure applications and finally also by connecting high numbers of small cells to 75/375 W-systems. As advantages, the company advertises fast start-up times and fuel flexibility. 

A. Kawakami, S. Matsuoka, N. Watanabe, A. Ueno, T. Ishihara, N. Sakai, K. Yamaji, H. Yokokawa, Development of low-temperature micro tubular type SOFC. Proceedings of the 13th Symposium on Solid Oxide Fuel Cells in Japan, 54-57 (2004)... 

T. Suzuki, Y. Funahashi, T. Yamaguchi, Y. Fujishiro, and M. Awano, Development of fabrication/integration technology for micro tubular SOFCs, in Micro Fuel Cells— Principles and Applications (Ed T.S. Zhao), Elsevier, Oxford, 2009, pp. 141-177. 

Cyclosporine is a macrolide antibiotic and has been used as an immunosuppressive agent. Cyclosporine can cause both renal and nonrenal toxicity. Clinically renal toxicity consists of four discrete syndromes which include acute reversible renal functional impairment, delayed renal allograft function, acute vasculopathy, and chronic nephropathy with interstitial fibrosis. Proximal tubular epithelium is uniquely sensitive to the toxic effect. The toxic effect is characterized by isometric cytoplasmic vacuolations (several small equally sized vacuoles in cytoplasm), necrosis with or without subsequent mineralization, inclusion bodies (giant mitochondria), and giant lysosomes. Acute vasculopathy consists of vacuolization of the arteriolar smooth muscles and endothelial cells leading to necrosis. In some cases, thrombotic microangiopathy develops, characterized by thrombosis of the renal micro vasculature. Long-term treatment with cyclosporine results in chronic nephropathy with interstitial fibrosis (Chamey et al., 2004). 

Studies of the pathophysiology of acute renal failure has classically considered both tubular and vascular mechanisms [227,228]. In vitro techniques isolating either the vascular or tubular components have been developed. For example, the use of isolated proximal tubules in suspension or in culture allows the study of tubular mechanisms of injury in the absence of vascular factors [229] [230]. There are both in vitro and in vivo models to study vascular injury in the kidney. In vitro models include the study of vascular smooth muscle cells or endothelial cells in culture. In this section, the in vivo methods to evaluate the renal micro-circulation will be discussed. This is of relevance as many nephrotoxins exert their deleterious effects through pharmacologic actions on the resistance vasculature with parenchymal injury occurring as a consequence of ischemia. In clinical practice nephrotoxins may cause prerenal azotemia as a result of increased renal vascular resistance. Nephrotoxins that cause acute renal failure on a vascular basis include prostaglandin inhibitors e.g. aspirin, non-steroidal anti-... 

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