For example, Kim et al. generated iPSCs from adult mouse and human neural stem cells by ectopic expression of a single transcription factor Oct4. As we previously demonstrated, a diverse range of neural stem markers including Sox2, were detected on LNS cells. The multipotent capability of limbal stroma derived stem/ progenitor cells have been reported by different research groups. Dravida et al. showed that stem cells derived from human corneal-limbal stroma, expressed the ESC marker SSEA-4 and other stem cell markers important for maintaining an undifferentiated state. Therefore, LNS cells may become an ideal cell resource for single-factor reprogramming and subsequent retinal repair due to their existing stem/progenitor cell properties, multipotency and plasticity. In summary, this data demonstrates the potential of mouse and human LNS to differentiate into retinal lineages in vitro and in vivo. The regulation of human LNS differentiation to a retinal lineage appears more comprehensive than with mouse LNS cells. As a readily accessible progenitor cell resource that can be derived from individuals up to 97 years of age, limbal neurosphere cells remain an attractive cell resource for the development of novel therapeutic approaches for degenerative retinal diseases. Moreover, in patients with HF, the development of AF significantly increases the risk of death. Thus, identifying and elucidating pharmacological targets to treat AF may significantly reduce mortality and morbidity in HF. It is well known that HF is a substrate for AF and these are common co-existing disease states. HF patients are at an increased risk for both atrial and ventricular arrhythmias, which contribute to morbidity and mortality. Our main findings were two-fold: first, we did not find any modulation of atrial myocyte repolarization by IKCa in the settings of normal, failing or sustained AF hearts. Secondly, IKCa is activated during HF contributing to stability of ventricular repolarization. Thus, block of IKCa in chronic HF ventricular myocytes prolonged repolarization and increased repolarization instability; these effects have been shown to predict proarrhythmia. Consistent with our findings, IKCa has been previously Everolimus suggested to play a protective role in the human ventricle during HF.. One interesting question is how IKCa becomes an important modulator of ventricular repolarization during heart failure. Potential explanations for this finding include 1) increased channel expression; 2) altered channel sensitivity to calcium; 3) increased calcium concentrations; or 4) loss of other repolarizing current, thereby unmasking the role of IKCa. In considering these possibilities, we observed an increase in SK3, but not SK2 in our canine HF model. However, we did not observe a statistically significant increase in either SK2 or SK3 in human HF, although there was a trend toward an increase in SK3 ; our findings are in contrast to a previous report where SK2 expression was increased in human HF. While the expression was not significantly increased in human HF, the interspecies differences we observed may be explained by the intrinsic enhanced variability in explanted human end-stage heart failure samples resulting from inhomogeneities in etiology, comorbidities and drug treatments.