An understanding of how chemoresistance arises in CSCs is likely to be important in the personalization of cancer therapy. We thank Tara Rambaldo for technical assistance with flow cytometry analysis, Linda Prentice for technical assistance in histological processing of samples, and Luda Urisman for technical assistance with maintenance of mouse inventory. We also thank Bishop and Chen lab members for helpful discussions. Additional Supporting Information may be found in the online version of this article. “
“The combination therapy of pegylated interferon-α and ribavirin (PEG IFN/RBV) is one of the effective

treatments for chronic hepatitis C (CHC) patients. Natural killer (NK)-cell activity was reported to be impaired in patients with hepatitis C virus (HCV). The aim of this study was to examine whether PEG IFN/RBV Bioactive Compound Library therapy could restore NK activity in CHC patients. In 19 CHC patients, PEG IFN/RBV therapy was performed. Just before (0M), at 3 months of the therapy (3M) and at 6 months after completion of the therapy (6M), NK activity and the frequency of NK cells, CD56dimNK cells and CD56brightNK cells in peripheral

blood was estimated by creatinine release assay and flow cytometry. Statistical analysis was performed by anova and Mann–Whitney U-test. anova showed Cilomilast molecular weight that NK activity significantly improved at 6M (vs 0M, P < 0.05) in the patients studied and in the patients with sustained virological response (SVR). It also showed that frequency

of CD56brightNK cells was significantly increased at 6M (vs 0M, P < 0.05) in the patients studied and PIK3C2G in the SVR group. However, no significant change in NK activity and frequency of CD56brightNK cells were detected in non-SVR group. Furthermore, NK activity ratio (6M/0M) in the SVR group was revealed to be higher compared with that in the non-SVR group by analysis using Mann–Whitney U-test (P < 0.05). PEG IFN/RBV therapy in CHC patients could improve NK activity by increasing the frequency of CD56brightNK cells in SVR patients. Our study also revealed that eradication of HCV could restore NK-cell activity. "
“The pathogenesis of type 2 diabetes is characterized by impaired insulin action and increased hepatic glucose production (HGP). Despite the importance of hepatic metabolic aberrations in diabetes development, there is currently no molecular probe that allows measurement of hepatic gluconeogenic pathways in vivo and in a noninvasive manner. In this study, we used hyperpolarized carbon 13 (13C)-labeled pyruvate magnetic resonance spectroscopy (MRS) to determine changes in hepatic gluconeogenesis in a high-fat diet (HFD)-induced mouse model of type 2 diabetes. Compared with mice on chow diet, HFD-fed mice displayed higher levels of oxaloacetate, aspartate, and malate, along with increased 13C label exchange rates between hyperpolarized [1-13C]pyruvate and its downstream metabolites, [1-13C]malate and [1-13C]aspartate.