• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2007.06a
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• pp.70-71
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• 2007

Analyzing pentacene field effect transistors (FETs) with Au source and drain electrodes as Maxwell-Wagner effect elements, electron and hole injection from the Au electrodes into the FET channel were examined using current-voltage (I-V), capacitance-voltage (C-V) and optical second harmonic generation (SHG) measurements. Based on these results, a mechanism of the hole and electron injection into pentacene from the Au electrodes and subsequently recombination mechanism with light-emitting in the pentacene layer are discussed, with taking into account the presence of trapped charges.

• Biomolecules & Therapeutics
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• v.10 no.1
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• pp.37-42
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• 2002

Brain drug targeting through the blood-brain barrier (BBB) in vivo is possible with peptidornirnetic monoclonal antibodies that undergo receptor-mediated transcytosis through the BBB. Monoclonal antibody to the rat transferrin receptor, such as the OX26 was studied in rats as a transport vector through BBB on the transferrin receptor. But, OX26 is not an effective brain delivery vector in mouse. In the present studies, rat monoclonal antibody, 8D3 to the mouse transferrin receptor were evaluated for brain drug targeting vector intransgenic mouse model. Pharrnacokinetic parameters in plasma and organ uptakes were determined at varioustimes after i.v. bolus injection of [$^{}125}I$] 8D3 in Balb/c mice. Brain uptake of [$^{}125}I$] 8D3 was also studied with an internal carotid artery perfusioncapillary depletion method. After i.v. injection of [$^{}125}I$] 8D3, plasma concentrations declined biexponentially with elimination half lift of approximately 2.2 hours. Brain uptake of [$^{}125}I$] 8D3 was $0.50{\pm}0.09$ persent of injected dose per g brain after 2 hours i.v. injection. After perfusion 5 min the apparent volume of distibution of [$^{}125}I$] 8D3 in brain was $22.3 {\mu}l/g,$ which was 4.8 fold higher than the intravascular volume. These studies indicate rat monoclonal antibody to the mouse transferrin receptor, 8D3 may be used for brain drug targeting vector in mice.

• Journal of Pharmaceutical Investigation
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• v.17 no.4
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• pp.213-216
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• 1987

The distribution features of recombinant human $alpha-interferon(rHuIFN-{\alpha}A)$ and $^{14}C-radiolabeled\;rHuIFN-{\alpha}A\;(^{14}C-rHuIFN-{\alpha}A)$ were investigated in ICR mice after i.v. injection. The level of $rHuIFN-{\alpha}A$ in the kidney was significantly higher than those in lung and liver at 10min after the injection. But the level was reduced significantly at 60min. The level of radioactivity in the kidney was also significantly higher than those in other organs after i.v. injection of $^{14}C-rHuIFN-{\alpha}A$, but it was reduced at much slower speed than was $rHuIFN-{\alpha}A$. These results show that interferon is distributed repidly and the kidney is the main site of distribution and metabolism of $rHuIFN-{\alpha}A$.

• Archives of Pharmacal Research
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• v.14 no.4
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• pp.290-294
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• 1991

For the determination of peripheral COMT activity, we synthesized $[2-^{14}C]-3',4'-dihydroxyacetophenone([^{14}C]-DHAP)$, a model substrate closely related to catecholamines, which cannot be attacked by monoamine oxidase. After i.v.-injection of $[^{14}C]-DHAP$ in living animals, only 3',4'-dihydroxy-acetophenone (3',4'-DHAP) and 3'-methoxy-4'-hydroxyacetophenone (3'-MHAP) were detected in blood by thin layer radio chromatography. It could be speculated that 3',4'-DHAP was primarily O-methylated by COMT, followed by subsequent conjugations. The concentration of 3',4'-DHAP, a substrate for COMT, in blood at 5 min after injection of $[^{14}C]-DHAP$, were similar in all animals. The rate of 3'-MHAP formation can be therefore used as an indicator for peripheral COMT activity. The velocity of methylation in 15 min after i.v.-administration of $[^{14}C]-DHAP$ was $0.28\;{\mu}g/ml{\cdot}min$. From these results, 3',4'-DHAP was shown to be used as an appropriate substrate to determine the COMT activity in vivo.

• YAKHAK HOEJI
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• v.45 no.4
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• pp.378-386
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• 2001

A purified histone Hl protein, p961, which plays a role in mediating the condensation of DNA into chromatin, was recently proved as an arthritis-suppressing agent in the mouse CIA model. The pharmacokinetics of p961 was carried out in rats and rabbits. The rat's blood, bile and urine samples were serially collected from the femoral vein, common bile duct, and bladder respectively, after bolus i.v. injection at low (10 mg/kg) and high (30 mg/mg) doses. The rabbit's blood samples were also collected from the marginal ear vein after bolus i.v. injection at a dose 10 mg/kg. p961 and its major metabolite in the physiological samples were analyzed by reverse-phase HPLC using a Yydac C4 protein column and a multistep water-acetonitrile gradient containing 0.24% trifluoroacetic acid. The major pharmacokinetic parameters (AUC, $C_{max}$, MRT, $t_{1}$2/, $V_{ss}$ and Cl) were estimated from the time course of plasma p961 and metabolite concentrations using WinNonlin. A two-compartment model was chosen for p961 as the most appropriate pharmacokinetic model. After i.v. injection of p961 at doses of 10 mg/kg and 30 mg/kg, more than 80% of p961 was removed rapidly from the plasma within 15 min. The plasma half-life of p961 in rats and rabbits was found not to exceed 12 min. p961 (22448.9 mol wt) was rapidly cleaved to 21612 mot wt fragment and the breakdown product appeared rapidly in the circulation with no lag phase. p961 and metabolite were not detected in rat urine and bile....

• Proceedings of the Korean Society Of Semiconductor Equipment Technology
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• 2003.12a
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• pp.45-49
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• 2003

본 논문에서는 gate 산화막을 위한 Hf oxide 박막을 $Hf(dmae)_4$ (dmae=dimethylaminoethoxide) 전구체로 Direct Liquid Injection Metal Organic Chemical Vapor Deposition (DLI-MOCVD)방법을 이용하여 p-type Si(100) 기판 위에 증착하였다. 이 전구체를 이용하여 $150^{\circ}C$의 낮은 증착 온도에서도 낮은 carbon 농도와 roughness를 가지는 양질의 박막을 증착할 수 있었다. 증착된 박막은 비정질 구조를 나타내었지만 annealing 온도를 증가시킴에 따라서 결정성(monoclinic phase)을 나타내었다. $500{\AA}$으로 증착한 박막을 C-V 와 I-V curve를 통하여 전기적 특성을 평가하였다. 열처리 온도가 증가함에 따라 유효유전상수(k)는 증가하지만 열처리 온도가 $900^{\circ}C$ 이상이 되면 계면층의 형성에 의해 유효유전상수는 감소하게 되고 이에 따라 누설 전류도 감소하게 된다. 산소분위기 $800^{\circ}C$에서 annealing한 $HfO_2$ 박막의 유전상수는 20.1이고, 누설 전류 밀도는 SV에서 $2.2\times10^{-6}A/\textrm{cm}^2$ 로 좋은 전기적 특성을 가진다.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.390-399
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• 2023

Background: Gintonin (GT), a Panax ginseng-derived lysophosphatidic acid receptor (LPAR) ligand, has positive effects in cultured or animal models for Parkinson's disease, Huntington's disease, and so on. However, the potential therapeutic value of GT in treating epilepsy has not yet been reported. Methods: Effects of GT on epileptic seizure (seizure) in kainic acid [KA, 55mg/kg, intraperitoneal (i.p.)]-induced model of mice, excitotoxic (hippocampal) cell death in KA [0.2 ㎍, intracerebroventricular (i.c.v.)]-induced model of mice, and levels of proinflammatory mediators in lipopolysaccharide (LPS)-induced BV2 cells were investigated. Results: An i.p. injection of KA into mice produced typical seizure. However, it was significantly alleviated by oral administration of GT in a dose-dependent manner. An i.c.v. injection of KA produced typical hippocampal cell death, whereas it was significantly ameliorated by administration of GT, which was related to reduced levels of neuroglial (microglia and astrocyte) activation and proinflammatory cytokines/enzymes expression as well as increased level of the Nrf2-antioxidant response via the upregulation of LPAR 1/3 in the hippocampus. However, these positive effects of GT were neutralized by an i.p. injection of Ki16425, an antagonist of LPA1-3. GT also reduced protein expression level of inducible nitric-oxide synthase, a representative proinflammatory enzyme, in LPS-induced BV2 cells. Treatment with conditioned medium clearly reduced cultured HT-22 cell death. Conclusion: Taken together, these results suggest that GT may suppress KA-induced seizures and excitotoxic events in the hippocampus through its anti-inflammatory and antioxidant activities by activating LPA signaling. Thus, GT has a therapeutic potential to treat epilepsy.

• The Korea Journal of Herbology
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• v.28 no.1
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• pp.83-90
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• 2013

Objectives : Tetramethylpyrazine (TMP) is an active ingredient in Ligusticum wallichii and has a wide range of neuroprotection effects. This study investigated anti-neuroinflammatory effect of TMP on brain regions in intracerebroventricular (i.c.v.) lipopolysaccharide (LPS)-treated C57BL/6 mice. Methods : TMP was administered intraperitoneally at doses of 10, 20, and 30 mg/kg at 1 h prior to LPS (3 mg/kg) i.c.v. injection. mRNA level of pro-inflammatory cytokines, including tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin (IL)-$1{\beta}$ and IL-6, was measured in the cerebral cortex, hippocampus, and hypothalamus tissue using real-time polymerase chain reaction at 24 h after the LPS injection. Cyclooxygenase-2 (COX-2) positive cells in the hypothalamus was also observed using immunohistochemistry at 24 h after the LPS injection. Results : At a dose of 30 mg/kg TMP significantly attenuated up-regulation of TNF-${\alpha}$ and IL-$1{\beta}$ mRNA in the cerebral cortex and IL-$1{\beta}$ mRNA in the hippocampus. In the hypothalamus, doses of 20 mg/kg and 30 mg/kg TMP significantly attenuated up-regulation of TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 mRNA induced by the LPS injection. In addition, TMP (30 mg/kg) significantly reduced the number of COX-2 positive cells in the hypothalamus. Conclusion : These results indicate that TMP has an anti-inflammatory effect on neuroinflammation, especially in the hypothalamus, induced by LPS i.c.v. injection and suggest that TMP-containing Ligusticum wallichii may play a modulatory role on the systemic responses following hypothalamic inflammation.

• Proceedings of the Korean Vacuum Society Conference
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• 2016.02a
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• pp.151.2-151.2
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• 2016

We characterized the n-type organic field-effect transistors (OFETs) with non-conjugated polyelectrolytes (NPEs) interlayers as the electron injection layer. Novel NPEs with various ions (Cl-, Br-, I-) improved the electron mobility from $5.06{\times}10^{-3}$ to $2.10{\times}10^{-2}cm^2V^{-1}s^{-1}$ in OFETs based [6,6]-Phenyl-$C_{61}$-butyric acid methyl ester (PCBM) when $PEIEH^+I^-$ spin-cast from 0.6% solution was deposited onto the PCBM layer. Reduced electron injection barrier (${\phi}_e$) at NPE/metal electrode interface was induced by dipole formation and led to increase the electron injection and transport. These findings are important for understanding how NPEs function in devices, the improvement of device performance, and the design of new materials for use in optoelectronic devices.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2001.07a
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• pp.45-49
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• 2001

We have investigated physical and electrical properties of the Hf $O_2$/HfS $i_{x}$/ $O_{y}$ thin film for alternative gate dielectrics in the metal-oxide-semiconductor device. The oxidation of Hf deposited directly on the Si substrate results in the H $f_{x}$/ $O_{y}$ interfacial layer and the high-k Hf $O_2$film simultaneously. Interestingly, the post-oxidation N2 annealing of the H102/H1Si70y thin films reduces(increases) the thickness of an amorphous HfS $i_{x}$/ $O_{y}$ layer(Hf $O_2$ layer). This phenomenon causes the increase of the effective dielectric constant, while maintaining the excellent interfacial properties. The hysteresis window in C-V curves and the midgap interface state density( $D_{itm}$) of Hf $O_2$/HfS $i_{x}$/ $O_{y}$ thin films less than 10 mV and ~3$\times$10$^{11}$ c $m^{-2}$ -eV without post-metallization annealing, respectively. The leakage current was also low (1$\times$10-s A/c $m^2$ at $V_{g}$ = +2 V). It is believed that these excellent results were obtained due to existence of the amorphous HfS $i_{x}$/ $O_{y}$ buffer layer. We also investigated the charge trapping characteristics using Fowler-Nordheim electron injection: We found that the degradation of Hf $O_2$/HfS $i_{x}$/ $O_{y}$ gate oxides is more severe when electrons were injected from the gate electrode.e electrode.e.e electrode.e.