Kumamoto University

About: Kumamoto University is a education organization based out in Kumamoto, Kumamoto, Japan. It is known for research contribution in the topics: Population & Cancer. The organization has 19602 authors who have published 35513 publications receiving 901260 citations. The organization is also known as: Kumamoto Daigaku.

Proton Conductivities of Graphene Oxide Nanosheets: Single, Multilayer, and Modified Nanosheets

Abstract: Proton conductivities of layered solid electrolytes can be improved by minimizing strain along the conduction path. It is shown that the conductivities (σ) of multilayer graphene oxide (GO) films (assembled by the drop-cast method) are larger than those of single-layer GO (prepared by either the drop-cast or the Langmuir-Blodgett (LB) method). At 60 % relative humidity (RH), the σ value increases from 1×10−6 S cm−1 in single-layer GO to 1×10−4 and 4×10−4 S cm−1 for 60 and 200 nm thick multilayer films, respectively. A sudden decrease in conductivity was observed for with ethylenediamine (EDA) modified GO (enGO), which is due to the blocking of epoxy groups. This experiment confirmed that the epoxide groups are the major contributor to the efficient proton transport. Because of a gradual improvement of the conduction path and an increase in the water content, σ values increase with the thickness of the multilayer films. The reported methods might be applicable to the optimization of the proton conductivity in other layered solid electrolytes.

Insulated gate and surface passivation structures for GaN-based power transistors

Abstract: Recent years have witnessed GaN-based devices delivering their promise of unprecedented power and frequency levels and demonstrating their capability as an able replacement for Si-based devices. High-electron-mobility transistors (HEMTs), a key representative architecture of GaN-based devices, are well-suited for high-power and high frequency device applications, owing to highly desirable III-nitride physical properties. However, these devices are still hounded by issues not previously encountered in their more established Siand GaAs-based devices counterparts. Metal–insulator–semiconductor (MIS) structures are usually employed with varying degrees of success in sidestepping the major problematic issues such as excessive leakage current and current instability. While different insulator materials have been applied to GaN-based transistors, the properties of insulator/III-N interfaces are still not fully understood. This is mainly due to the difficulty of characterizing insulator/AlGaN interfaces in a MIS HEMT because of the two resulting interfaces: insulator/AlGaN and AlGaN/GaN, making the potential modulation rather complicated. Although there have been many reports of low interface-trap densities in HEMT MIS capacitors, several papers have incorrectly evaluated their capacitance–voltage (C–V) characteristics. A HEMT MIS structure typically shows a 2-step C–V behavior. However, several groups reported C–V curves without the characteristic step at the forward bias regime, which is likely to the high-density states at the insulator/ AlGaN interface impeding the potential control of the AlGaN surface by the gate bias. In this review paper, first we describe critical issues and problems including leakage current, current collapse and threshold voltage instability in AlGaN/GaN HEMTs. Then we present interface properties, focusing on interface states, of GaN MIS systems using oxides, nitrides and high-κ dielectrics. Next, the properties of a variety of AlGaN/GaN MIS structures as well as different characterization methods, including our own photo-assisted C–V technique, essential for understanding and developing successful surface passivation and interface control schemes, are given in the subsequent section. Finally we highlight the important progress in GaN MIS interfaces that have recently pushed the frontier of nitride-based device technology.

Spindle checkpoint function is required for mitotic catastrophe induced by DNA-damaging agents

Abstract: Mitotic catastrophe is an important mechanism for the induction of cell death in cancer cells by antineoplastic agents that damage DNA. This process is facilitated by defects in the G1 and G2 checkpoints of the cell cycle that are apparent in most cancer cells and which allow the cells to enter mitosis with DNA damage. We have now characterized the dynamics of mitotic catastrophe induced by DNA-damaging agents in p53-deficient cancer cells. Cells that entered mitosis with DNA damage transiently arrested at metaphase for more than 10 h without segregation of chromosomes and subsequently died directly from metaphase. In those metaphase arrested precatastrophic cells, anaphase-promoting complex appeared to be inactivated and BubR1 was persistently localized at kinetochores, suggesting that spindle checkpoint is activated after the DNA damage. Furthermore, suppression of spindle checkpoint function by BubR1 or Mad2 RNA interference in the DNA damaged cells led to escape from catastrophic death and to subsequent abnormal mitosis. Dysfunction of the spindle checkpoint in p53-deficient cancer cells is thus likely a critical factor in resistance to DNA-damaging therapeutic agents.

Dilated Cardiomyopathy Caused by Aberrant Endoplasmic Reticulum Quality Control in Mutant KDEL Receptor Transgenic Mice

Abstract: Aberrant protein folding beyond the capacity of endoplasmic reticulum (ER) quality control leads to stress response in the ER. The Lys-Asp-Glu-Leu (KDEL) receptor, a retrieval receptor for ER chaperones in the early secretory pathway, contributes to ER quality control. To elucidate the function of the KDEL receptor in vivo, we established transgenic mice expressing a mutant KDEL receptor. We found that the mutant KDEL receptor sensitized cells to ER stress and that the mutant mice developed dilated cardiomyopathy. Ultrastructural analyses revealed expanded sarcoplasmic reticulums and protein aggregates that obstructed the adjacent transverse tubules of the mutant cardiomyocytes. Cardiomyocytes from the mutant mice were sensitive to ER stress when treated with tunicamycin and showed a functional defect in the L-type Ca2+ current. We observed ubiquitinated protein aggregates, enhanced expression of CHOP (a death-related transcriptional factor expressed upon ER stress), and apoptosis in the mutant hearts. These findings suggest that impairment of the KDEL receptor disturbs ER quality control, resulting in accumulation of misfolded proteins in the ER in an in vivo system, and that the dilated cardiomyopathy found in the mutant KDEL receptor transgenic mice is associated with ER stress.

Nf1 has an essential role in endothelial cells

Abstract: Neurofibromatosis type 1 (NF1) or von Recklinghausen neurofibromatosis is a genetic disorder that occurs in 1 of 4000 births and is characterized by benign and malignant tumors. Cardiovascular defects also contribute to NF1, though the pathogenesis is still unclear. Deficiency in neurofibromin (encoded by Nf1) in mice results in mid-embryonic lethality owing to cardiac abnormalities previously thought to be secondary to cardiac neural-crest defects. Using tissue-specific gene inactivation, we show that endothelial-specific inactivation of Nf1 recapitulates key aspects of the complete null phenotype, including multiple cardiovascular abnormalities involving the endocardial cushions and myocardium. This phenotype is associated with an elevated level of ras signaling in Nf1−/− endothelial cells and greater nuclear localization of the transcription factor Nfatc1. Inactivation of Nf1 in the neural crest does not cause cardiac defects but results in tumors of neural-crest origin resembling those seen in humans with NF1. These results establish a new and essential role for Nf1 in endothelial cells and confirm the requirement for neurofibromin in the neural crest.