Trp155 is not conserved in any if the bacterial genomes available at present, while the appearance of Phe at equivalent position to Phe150 is rare. Thermophilic enzymes frequently present increased number of clustered aromatic residues, which are often mutated to Leu in the mesophilic counterparts, as is the case in cvPAH. Surfaceexposed small aromatic clusters, often located close to the active sites, have been found to confer an entropic advantage over mesophilic analogues through generation of low-frequency motions. Based on the high sequence identity with the other PAH enzymes of known 3D-structure, Trp155 would be located at the start of the helix leading to the iron-coordinating residue Glu167 and might form a stabilizing aromatic cluster with Phe150 and/or Phe92. Furthermore, it is also well established that oligomerization is a strong stabilization mechanism and a large proportion of hyperthermophilic proteins have a higher oligomerization state than their mesophilic counterparts. In this context it is interesting that thermostable lpPAH appears to be dimeric, while other purified and characterized bacterial PAHs are monomeric. The clinical Butenafine hydrochloride symptoms and signs of ARF manifest as a rapid loss of the ability of the kidneys to excrete wastes, concentrate urine, and maintain fluid and electrolyte homeostasis. In pathophysiology, ARF may result from prolonged renal hypoperfusion and renal ischemia or nephrotoxic substances, and is associated with tubular cell death and shedding of cells into the tubular lumen, resulting in tubular blockage and further decreasing glomerular filtration. The overall mortality rate of patients with ARF is still high despite major advances in pharmacologic therapy, intensive care, and renal replacement therapy. Therefore, a more potent therapeutic intervention for ARF to reduce mortality is imperative. Our previous study showed that endogenous bone marrow cells could contribute to the renal tubular epithelial cell population and regeneration of the renal tubular epithelium by DNA synthesis after folic acid-induced acute kidney injury, although most of the renal tubular regeneration came from indigenous cells. These results have also been supported by another study. Recently, a stem cell-based treatment strategy has started to become a realistic option to replace or rebuild damaged organs and tissues. Stem cell therapy has been successfully applied using a variety of cell types, including mesenchymal stem cells, BM cells, and human umbilical cord blood cells, to rescue organ Albaspidin-AA damage in animal and human studies. On the basis of studies of allogeneic BM MSCs as a cell source for stem cell therapy for acute tubular necrosis, several studies have shown that sorted BM MSCs can rescue nonirradiated mice from acute renal tubular damage caused by toxins or ischemia; however, it is still debatable whether the beneficial effects of MSCs are primarily mediated via their differentiation into target cells, or by complex paracrine actions. BM MSCs are obtained from human bone marrow; however, aspiration of BM is an invasive procedure, and the numbers and differentiation capabilities of BM MSCs decline significantly with age. Fetal MSCs are derived from fetuses, a source associated with considerable ethical problems for human application, making these cells difficult to obtain. Compared with BM MSCs and fetal MSCs, human umbilical cord-derived mesenchymal stem cells can be separated from discarded umbilical cord, which causes no harm to the donor, and is not ethically problematic. Therefore, hUC-MSCs are a safe and accessible source for large quantities of stem cells in comparison to fetal MSCs and BM MSCs.