The cause of death from selleck chemical the toxic liver injury was not characterized, correction of any specific liver function by the engrafted

cells was not demonstrated, and whether the iPSC-derived hepatocytes responded appropriately to proliferation signals after loss of hepatocyte mass was not tested. In summary, the recent findings by Takebe et al. offer encouragement for the use of PSC-derived hepatocytes for tissue engineering. Nevertheless, it is important to recognize that a combination of vasculature, stromal cells, and hepatocytes does not an organ make. Liver architecture, including biliary structures, is critical for the liver’s exocrine function. Liver-like tissues have been generated from primary rodent and human hepatocytes,[11, 12] and primary hepatocytes that have colonized

lymph nodes can produce enough ectopic liver mass to rescue a mouse from a lethal metabolic disease, indicating that the lymph node contains enough structure for primary selleck screening library cells to support liver tissue and life-sustaining organ function. It may also be important to consider that nonparenchymal cells could have organ-specific characteristics that potentially have unique roles in controlling organ development and function.[14] Transplant of iPSC-derived liver buds into the native hepatic environment may therefore prove to be efficacious and could potentially promote cholangiocyte differentiation. The potential to generate organs from iPSCs is exciting and could have substantial ramification for the treatment of liver disease; however, more complete differentiation

of iPSCs to a mature hepatic phenotype with the capacity to expand as robustly as primary human hepatocytes will be required. Long-term engraftment in host animals has long been thought to be the most likely way to produce near-complete maturation of iPSC-derived hepatocytes. A significant finding from this study is that, unlike iPSC-derived pancreatic beta cells, the iPSC-derived hepatocytes in the cell clusters failed to completely differentiate after transplantation in immune-deficient adult hosts.[13] Thus, many important positive and negative lessons can be taken from this work, and, with them, many more questions will need answers. The authors thank Dr. Jayanta Roy-Chowdhury for his see more careful review of the manuscript and helpful suggestions. Ira J. Fox, M.D.1 “
“Background and Aim:  A number of hepatitis C virus (HCV) patients without a rapid virological response (RVR) achieved a sustained virological response (SVR) with peginterferon-α-2a/ribavirin. The aim of this study was to identify factors associated with SVR in non-RVR patients. Methods:  Baseline and on-treatment factors were used to explore the prognostic factors for SVR in 113 HCV genotype-1 (HCV-1) and 20 HCV-2 non-RVR patients in two randomized trials.