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Organic-inorganic hybrid co-polymer thin films were deposited on silicon(100) substrates under the several ratio of TEOS (tetraethoxysilane) against toluene by plasma enhanced chemical vapour deposition (PECVD) method. Toluene and TEOS were utilized as organic and inorganic precursors each, and hydrogen and argon were also used as a bubbler and carrier gases, respectively. In order to compare the difference of the electrical and the mechanical properties of the plasma polymerized thin films, we grew the hybrid co-polymer thin films under the conditions of various ratio between toluene and TEOS with fixed RF (radio frequency using 13.56 MHz) powers at 30 W. The as-grown polymerized thin films were in first analyzed by FT-IR and XPS. The result of FT-IR showed that the co-polymer thin films were polymerized with fragmented each precursor. Also, XPS results showed the chemical species and binding energies of each species. Si 2p core-level spectra from the hybrid polymer thin film showed the status of Si oxidation number. Impedance analyzer was utilized for the measurements of I-V curves and capacitance values. Also, the thin films were analyzed for hardness and Young's modulus by nano-indenter.

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Huntington's disease (HD) is an autosomal-dominant neurological disorder caused by expanded CAG repeats in the Huntingtin (Htt) gene, but it is not known how this mutation causes neurodegeneration. Herein, we found that dysfunction of upstream binding factor-1 (UBF-1) is linked to reduced ribosomal DNA (rDNA) transcription in HD. We identified that UBF1 acetylation at Lys (K) 352 by CREB binding protein (CBP) is crucial for the transcriptional activity of rDNA. UBF1 mutation (K352A, K352Q, and K352R) decreased rDNA transcriptional activity. Moreover, both CBP-dHAT mutant and knockdown of CBP by siRNA reduced acetylation of UBF1 and resulted in the decreased transcription of rDNA into rRNA. ChIP analysis showed a significant reduction of UBF1 occupancy in the promoter of rDNA in STHdh(Q111) cell line model of HD. These results demonstrate that abnormal activity of UBF1 and its acetylation by CBP are linked to impaired rDNA transcription in HD. This novel mechanism suggests that modulation of UBF-mediated rDNA synthesis by CBP may be a therapeutic target for improving neuronal rDNA transcription in HD.

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Single-crystalline and epitaxial cubic silicon carbide (beta-SiC) nano-thin films have been deposited on Si(100) substrates at a sample temperature of approximately 900 degrees C using single source precursors by the thermal metal-organic chemical vapor deposition (MOCVD) method. Diethylmethylsilane and 1,3-disilabutane, which contain Si and C atoms in the same molecule, were used as precursors without any carrier or bubbler gas. Upon increasing the deposition temperature from 900 to 950 degrees C, beta-SiC nano-thin films with relatively small crystals and smoother surfaces were created on Si(100) substrates. Moreover, beta-SiC nano-wires with 40 approximately 100 nm in diameter have also been grown selectively on nickel catalyzed Si(100) substrates with dichloromethylvinylsilane by the MOCVD method. The deposition temperature in this case was as low as 800 degrees C under the pressure of 5.0 x 10(-2) Torr. It is worth noting that the initial growth rates of deposited beta-SiC nano-thin films and nano-wires strongly depend on the deposition temperature rather than the time. In order to test the possibility of applications of these materials for electronic components such as field emitter, MEMS, and high-power transistor, we fabricated the nanoelectronic devices using both beta-SiC nano-wires and nano-thin films. With these preliminary application tests, it is expected that SiC nanowires can be used as field emitter and nanoelectronic high-power transistor, and application of the SiC nano-thin films to MEMS is promising as well.

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Caspase-12 is activated when the cells are exposed to excess levels of various stimuli, which cause endoplasmic reticulum (ER) stress. Protein kinase C (PKC) plays an important role in many signaling pathways in cells, and the activation of PKC has multiple actions in the signaling function of the ER. This study examined whether or not phorbol 12, 13-dibutyrate (PDBu)-induced PKC activation modulates caspase-12 cleavage and it's processing, using a wild type caspase-12 overexpressing neuronal cell line, known as Cas-12 cells. The thapsigargin treatment induced caspase-12 fragmentation in the Cas-12 cells. This was inhibited by PKC, which had previously been stimulated by PDBu. The PDBu treatment attenuated the ER stress-induced translocation of caspase-12 from the ER to the cytoplasm. The caspase-3 specific inhibitor blocked caspase-12 fragmentation, and purified caspase-12 was cleaved by the active caspase-3 in vitro, suggesting that caspase-12 might be a substrate for caspase-3. In addition, the PDBu treatment influenced the decrease of active caspase-3 fragment. These results suggest that an ER stress induces the activation of caspase-12 via caspase-3, and that PKC regulates both caspase-12 and caspase-3 activations in Cas-12 cells.

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Neurons, but not astrocytes, are known as the major source of Abeta, because astrocytes express low levels of putative beta-secretase (BACE). Astrocytes near senile plaque cores show enhanced levels of BACE protein expression, however, suggesting that astrocytes can contribute to Abeta production under pathological conditions. To investigate factors that stimulate BACE protein expression in astrocytes, we tested the effects of interleukin-1beta (IL-1beta) and interferon-gamma (IFN-gamma) on BACE protein expression in U373MG astrocytoma cells and primary astrocyte cultures from Tg2576 mouse brains. BACE protein expression and sAPPbeta production were dramatically increased, without changes in holo APP levels, following IFN-gamma treatment in both cell types. AG490, which is a blocker of IFN-gamma-induced STAT signaling, decreased IFN-gamma-induced BACE protein expression and sAPPbeta production in a dose-dependent manner. These results show that astrocytes are capable of expressing BACE and producing sAPPbeta in response to certain stimulating factors, and IFN-gamma is one such factor.

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We investigated the cognition enhancing effects of ginsenoside Rb1 and Rg1. Mice were trained in a Morris water maze following injection (i.p.) of Rb1 (1 mg/kg) or Rg1 (1 mg/kg) for 4 days. Both Rb1- and Rg1-injected mice showed enhanced spatial learning compared to control animals. The hippocampus, but not the frontal cortex, of treated mice contained higher density of a synaptic marker protein, synaptophysin, compared to control mice. Electrophysiological recordings in hippocampal slices revealed that Rb1 or Rg1 injection did not change the magnitude of paired-pulse facilitation or long-term potentiation. Our results suggest that Rb1 and Rg1 enhance spatial learning ability by increasing hippocampal synaptic density without changing plasticity of individual synapses.

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