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Continuing CMOS performance scaling requires developing MOSFETs of high-mobility semiconductors and InGaAs is a strong candidate for n-channel. InGaAs MOSFETs, however, suffer from high densities of border traps, and their origin and impact on device characteristics are poorly understood at present. In this paper, the border traps in nMOSFETs with an In0.53Ga0.47As channel and Al2O3 gate oxide are investigated using the discharging-based energy profiling technique. By analyzing the trap energy distributions after charging under different gate biases, two types of border traps together with their energy distributions are identified. Their different dependences on temperature and charging time support that they have different physical origins. The impact of channel thickness on them is also discussed. Identifying and understanding these different types of border traps can assist in the future process optimization. Moreover, border trap study can yield crucial information for long-term reliability modeling and device time-to-failure projection. [ABSTRACT FROM AUTHOR]

Presents an interview with Chinese reading teacher Daisy Zhou, about reading education in China and the United States. Zhou's introduction to English; Whole language principles used in teaching; Disagreement about teaching English in China; Importance of teaching materials; Ideas for teaching Chinese immigrant students.

Hepatocellular carcinoma (HCC) is one of the leading cancers in the world in incidence and mortality. Current pharmacotherapy of HCC is limited in the number and efficacy of anticancer agents. Metabolic reprogramming is a prominent feature of many cancers and has rekindled interest in targeting metabolic proteins for cancer therapy. Glycogen is a storage form of glucose, and the levels of glycogen have been found to correlate with biological processes in reprogrammed cancer cells. However, the contribution of glycogen metabolism to carcinogenesis, cancer cell growth, metastasis, and chemoresistance is poorly understood. Thus, we studied the processes involved in the inhibition of glycogen metabolism in HCC cells. Pharmacological inhibition of glycogen phosphorylase (GP), a rate-limiting enzyme in glycogen catabolism, by CP-91149 led to a decrease in HCC cell viability. GP inhibition induced cancer cell death through the intrinsic apoptotic pathway. Mitochondrial dysfunction and autophagic adaptations accompanied this apoptosis process whereas endoplasmic reticulum stress, necrosis, and necroptosis were not major components of the cell death. In addition, GP inhibition potentiated the effects of multikinase inhibitors sorafenib and regorafenib, which are key drugs in advanced-stage HCC therapy. Our study provides mechanistic insights into cell death by perturbation of glycogen metabolism and identifies GP inhibition as a potential HCC pharmacotherapy target. Image 1 • Glycogen phosphorylase (GP) inhibition induces intrinsic apoptosis in liver cancer cells. • Mitochondrial dysfunctions- ROS generation and loss of MMP accompany apoptosis. • Autophagic adaptations are observed upon GP inhibition. • GP inhibition potentiates multikinase inhibitors in liver cancer cells. [ABSTRACT FROM AUTHOR]