National Cheng Kung University

About: National Cheng Kung University is a education organization based out in Tainan City, Taiwan. It is known for research contribution in the topics: Population & Thin film. The organization has 49723 authors who have published 69799 publications receiving 1437420 citations. The organization is also known as: NCKU.

Influence of an electric field on the optical properties of few-layer graphene with AB stacking

Abstract: The effect of perpendicular electric field F on optical properties of the AB-stacked few-layer graphene, made up of two, three, or four graphite sheets, is explored through the gradient approximation. In contrast to the featureless optical spectra of graphene, the low-energy absorption spectra of few-layer graphene with AB stacking exhibit many jumping structures, which result from the band-edge states caused by the stacking effect, in the absence of an electric field. Remarkably, F causes the subband anticrossing, changes the subband spacing, produces the oscillating bands, and increases the band-edge states. It, therefore, follows that the field-modulating spectra with sharp peaks are generated. Moreover, the frequency of peak, which is strongly dependent on the layer number and the field strength, is predicted. Above all, the predicted absorption spectra and the associated electronic properties could be verified by the optical measurements.

Different Types of Ground Glass Hepatocytes in Chronic Hepatitis B Virus Infection Contain Specific Pre-S Mutants that May Induce Endoplasmic Reticulum Stress

Abstract: Ground glass hepatocyte (GGH) represents a histological hallmark of chronic hepatitis B virus infection and contains surface antigens in the endoplasmic reticulum (ER). Several types of GGHs are recognized at different hepatitis B virus replicative stages. The recent identification of pre-S mutants from GGHs encourages us to investigate whether different GGHs may harbor specific mutants and exhibit differential biological activities. In this study, we applied laser capture microdissection to isolate specific GGHs from a total of 50 samples on eight resected liver specimens. The surface genes in two major types of GGHs were analyzed. Type I GGHs expressed an inclusion-like pattern of hepatitis B surface antigens and harbored mutants with deletions over pre-S1 region, whereas type II GGHs, distributed in clusters and emerged at late replicative phase, contained mutants with deletions over pre-S2 region that defines a cytotoxic T lymphocyte (CTL) immune epitope, and may represent an immune escape mutant. Transfection of pre-S mutants in Huh7 revealed decreased syntheses of middle and small S proteins with accumulation of large surface antigen in ER, which in turn led to the activation of ER stress response with differential activities for different mutants. This study therefore demonstrates that different GGHs may contain specific mutants and exhibit differential biological activities.

Downregulation of CREB expression in Alzheimer's brain and in Aβ-treated rat hippocampal neurons.

Abstract: Oxidative stress plays an important role in neuronal dysfunction and neuron loss in Alzheimer's brain. Previous studies have reported downregulation of CREB-mediated transcription by oxidative stress and Aβ. The promoter for CREB itself contains cyclic AMP response elements. Therefore, we examined the expression of CREB in the hippocampal neurons of Tg2576 mice, AD post-mortem brain and in cultured rat hippocampal neurons exposed to Aβ aggregates. Laser Capture Microdissection of hippocampal neurons from Tg2576 mouse brain revealed decreases in the mRNA levels of CREB and its target, BDNF. Immunohistochemical analysis of Tg2576 mouse brain showed decreases in CREB levels in hippocampus and cortex. Markers of oxidative stress were detected in transgenic mouse brain and decreased CREB staining was observed in regions showing abundance of astrocytes. There was also an inverse correlation between SDS-extracted Aβ and CREB protein levels in Alzheimer's post-mortem hippocampal samples. The levels of CREB-regulated BDNF and BIRC3, a caspase inhibitor, decreased and the active cleaved form of caspase-9, a marker for the intrinsic pathway of apoptosis, was elevated in these samples. Exposure of rat primary hippocampal neurons to Aβ fibrils decreased CREB promoter activity. Decrease in CREB mRNA levels in Aβ-treated neurons was reversed by the antioxidant, N-acetyl cysteine. Overexpression of CREB by adenoviral transduction led to significant protection against Aβ-induced neuronal apoptosis. Our findings suggest that chronic downregulation of CREB-mediated transcription results in decrease of CREB content in the hippocampal neurons of AD brain which may contribute to exacerbation of disease progression.