• Advances in nano research
• /
• v.5 no.3
• /
• pp.261-279
• /
• 2017

Spectroscopic investigation of Si quantum dots (Si-QDs) embedded in silicon nitride was performed over a broad stoichiometry range to optimize light emission. Plasma-enhanced chemical vapor deposition was used to grow the $SiN_x$ films on Si (001) substrates. The film composition was controlled via the flow ratio of silane ($SiH_4$) and ammonia ($NH_3$) in the range of R = 0.45-1.0 allowed to vary the Si excess in the range of 21-62 at.%. The films were submitted to annealing at $1100^{\circ}C$ for 30 min in nitrogen to form the Si-QDs. The properties of as-deposited and annealed films were investigated using spectroscopic ellipsometry, Fourier transform infrared spectroscopy, Raman scattering and photoluminescence (PL) methods. Si-QDs were detected in $SiN_x$ films demonstrating the increase of sizes with Si excess. The residual amorphous Si clusters were found to be present in the films grown with Si excess higher than 50 at.%. Multi-component PL spectra at 300 K in the range of 1.5-3.5 eV were detected and nonmonotonous varying total PL peak versus Si excess was revealed. To identify the different PL components, the temperature dependence of PL spectra was investigated in the range of 20-300 K. The analysis allowed concluding that the "blue-orange" emission is due to the radiative defects in a $SiN_x$ matrix, whereas the "red" and "infrared" PL bands are caused by the exciton recombination in crystalline Si-QDs and amorphous Si clusters. The nature of radiative and no radiative defects in $SiN_x$ films is discussed. The ways to control the dominant PL emission mechanisms are proposed.

• Journal of the Korean Chemical Society
• /
• v.33 no.5
• /
• pp.468-476
• /
• 1989

Kineties for the reactions of pyridines with 1-anthracenesulfonyl chloride (1-ASC) and 3-phenanthrenesulfonyl chloride (3-PSC) was investigated in methanol as solvent. Structural variation in pyridine followed $Br{\o}$ nsted and Hammett relations for both 1-ASC and 3-PSC; the corresponding coefficients, {\beta}\;and\;{\rho}\;at\;20^{\circ}C$ were 0.55, -3.5 for 1-ASC, and 0.43, -2.6 for 3-PSC respectively. Reactivity-selectivity principle was checked in competition system 1-ASC/3-PSC. As a result, this principle was found to hold at experimental temperatures, whereas to break down over in the range of isoselective temperature ($34.3^{\circ}C$). Judging from the above results and activation parameters, we concluded that these reactions proceeded by synchronous $S_n2$ mechanism in rate-determining step.

• Journal of the Korean Chemical Society
• /
• v.24 no.1
• /
• pp.44-52
• /
• 1980

Ionic dissociation rates of $\alpha$-chlorobenzyl ethyl ether in each solvent of toluene-$d_8$ and carbon tetrachloride were measured by the method of dynamic NMR spectroscopy. The spin system of these 1H NMR spectra was $AB_3$. The theoretical spectrum was calculated by computer simulation of dynamic NMR spectra, which agreed very well with observed spectra. From this computer simulation, the ionic dissociation rate constant k was obtained, and by Eyring plot with it, slope and intercept length was gained, from which kinetic parameters were calculated.The easiness of ionic dissociation depended upon solvent polarity. Activation enthalpy was 4.7 kcal/mole in toluene-$d_8$, 10.7 kcal/mole in carbon tetrachloride, and activation entropy was -35. 8 e.u. in toluene-$d_8$, -14.4 e.u. in carbon tetrachloride. It was understood that though the ${\Delta}H^{neq}$ value was small, this ionic dissociation had an easier procession in nonpolar solvents with increasing temperatures. Considering that the ionic dissociation could be thought as the first step of $S_N1$ mechanism, attention might be paid to the results that the value of ${\Delta}S^{neq}$ had a large negative value in comparison with a small ${\Delta}H^{neq}$.

• Proceedings of the Korean Society of Machine Tool Engineers Conference
• /
• 2003.04a
• /
• pp.398-404
• /
• 2003

Most previous researches for the hybrid composite materials such as FRMLs(Al/AFRP, Al/GFRP) have evaluated the fatigue delamination behavior using the traditional fracture mechanism. However, most previous researches have not generally been firmed yet. Because delamination growth behavior in hybrid composite should be consider delamination growth rate, $dA_D$/da using the delamination shape factors, fs instead of traditional fracture mechanic parameters. The major purpose of this study was to evaluate the relationship between delamination shape factor, fs and delamination growth rate, $dA_D$ . And a propose parameter on the delamination aspect ratio, b/a. The details of the study are as follow : 1) Relationship between crack length, a and delamination width,b. 2) Relationship between delamination aspect ration, b/a and delamination area rate,($(A_D)_{N}(A_D)_{ALL}$. 3) Variation of delamination growth rate, $dA_D/da$ was attendant on delamination shape factors, $fs_1$, $fs_2$, $fs_3$. The test results indicated the delamination growth rate depends on delamination shape factors.

• Bulletin of the Korean Chemical Society
• /
• v.35 no.8
• /
• pp.2371-2374
• /
• 2014

A kinetic study is reported on SNAr reaction of 1-fluoro-2,4-dinitrobenzene with a series of primary amines including hydrazine in $H_2O$ at $25.0^{\circ}C$. The plots of $k_{obsd}$ vs. [amine] are linear and pass through the origin, indicating that general-base catalysis by a second amine molecule is absent. The Br${\o}$nsted-type plot exhibits an excellent linear correlation with ${\beta}_{nuc}$ = 0.46 when hydrazine is excluded from the correlation. The reaction has been suggested to proceed through a stepwise mechanism, in which expulsion of the leaving group occurs after the rate-determining step (RDS). Hydrazine is ca. 10 times more reactive than similarly basic glycylglycine (i.e., the ${\alpha}$-effect). A five-membered cyclic intermediate has been suggested for the reaction with hydrazine, in which intramolecular H-bonding interactions would facilitate expulsion of the leaving group. However, the enhanced leaving-group ability is not responsible for the ${\alpha}$-effect shown by hydrazine because expulsion of the leaving group occurs after RDS. Destabilization of the ground-state of hydrazine through the electronic repulsion between the nonbonding electron pairs is responsible for the ${\alpha}$-effect found in the current $S_NAr$ reaction.

• Journal of the Korean institute of surface engineering
• /
• v.35 no.1
• /
• pp.33-38
• /
• 2002

For the evaluation of nucleation and growth behaviors influenced by substrate properties, such as surface energy, structure and electrical properties, chromium nitride films (CrN) were deposited on various substrates (glass, AISI 1040 steel and Si (110) by unbalanced magnetron sputtering. X-ray diffraction and Atomic Force Microscopy (AFM) were used to study the microstructure and grain growth as a function of deposition time. The diffraction patterns of CrN thin films deposited on Si (110) exhibited crystalline structure with highly preferred orientation of (200) plane parallel to the substrate, whereas the films deposited on glass and AISI 1040 exhibited preferred orientations (200) and minor orientation (111), (311) or (220) plane. The orientation of films deposited both on glass and Si substrates did not depend on the bias voltage (Vs). The grain growth and structure of film deposited on AISI 1040 steel substrate are strongly influenced by the substrate bias in comparison with that deposited onto glass and Si substrates. The differences in the structure and grain growth of CrN films deposited onto different substrates are predominantly related to the properties of the substrate (structure and electrical conductivity).

• Journal of Ginseng Research
• /
• v.41 no.3
• /
• pp.392-402
• /
• 2017

Background: Previously, we reported that Korean Red Ginseng inhibited liver fibrosis in mice and reduced the expressions of fibrogenic genes in hepatic stellate cells (HSCs). The present study was undertaken to identify the major ginsenoside responsible for reducing the numbers of HSCs and the underlying mechanism involved. Methods: Using LX-2 cells (a human immortalized HSC line) and primary activated HSCs, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide) assays were conducted to examine the cytotoxic effects of ginsenosides. $H_2O_2$ productions, glutathione contents, lactate dehydrogenase activities, mitochondrial membrane permeabilities, apoptotic cell subpopulations, caspase-3/-7 activities, transferase dUTP nick end labeling (TUNEL) staining, and immunoblot analysis were performed to elucidate the molecular mechanism responsible for ginsenoside-mediated cytotoxicity. Involvement of the AMP-activated protein kinase (AMPK)-related signaling pathway was examined using a chemical inhibitor and small interfering RNA (siRNA) transfection. Results and conclusion: Of the 11 ginsenosides tested, 20S-protopanaxadiol (PPD) showed the most potent cytotoxic activity in both LX-2 cells and primary activated HSCs. Oxidative stress-mediated apoptosis induced by 20S-PPD was blocked by N-acetyl-$\text\tiny L$-cysteine pretreatment. In addition, 20S-PPD concentration-dependently increased the phosphorylation of AMPK, and compound C prevented 20S-PPD-induced cytotoxicity and mitochondrial dysfunction. Moreover, 20S-PPD increased the phosphorylation of liver kinase B1 (LKB1), an upstream kinase of AMPK. Likewise, transfection of LX-2 cells with LKB1 siRNA reduced the cytotoxic effect of 20S-PPD. Thus, 20S-PPD appears to induce HSC apoptosis by activating LKB1-AMPK and to be a therapeutic candidate for the prevention or treatment of liver fibrosis.

• Journal of Life Science
• /
• v.26 no.3
• /
• pp.376-386
• /
• 2016

Apoptosis induction has been proposed as an efficient mechanism by which malignant tumor cells can be removed following chemotherapy. The intrinsic mitochondria-dependent apoptotic pathway is frequently implicated in chemotherapy-induced tumor cell apoptosis. Since DNA-damaging agent (DDA)-induced apoptosis is mainly regulated by the tumor suppressor protein p53, and since more than half of clinical cancers possess inactive p53 mutants, microtubule-damaging agents (MDAs), of which apoptotic effect is mainly exerted via p53-independent routes, can be promising choice for cancer chemotherapy. Recently, we found that the apoptotic signaling pathway induced by MDAs (nocodazole, 17α-estradiol, or 2-methoxyestradiol) commonly proceeded through mitotic spindle defect-mediated prometaphase arrest, prolonged Cdk1 activation, and subsequent phosphorylation of Bcl-2, Mcl-1, and Bim in human acute leukemia Jurkat T cells. These microtubule damage-mediated alterations could render the cellular context susceptible to the onset of mitochondria-dependent apoptosis by triggering Bak activation, Δψm loss, and resultant caspase cascade activation. In contrast, when the MDA-induced Bak activation was inhibited by overexpression of anti-apoptotic Bcl-2 family proteins (Bcl-2 or Bcl-xL), the cells in prometaphase arrest failed to induce apoptosis, and instead underwent mitotic slippage and endoreduplication cycle, leading to formation of populations with 8N and 16N DNA content. These data indicate that cellular apoptogenic mechanism is critical for preventing polyploid formation following MDA treatment. Since the formation of polyploid cells, which are genetically unstable, may cause acquisition of therapy resistance and disease relapse, there is a growing interest in developing new combination chemotherapies to prevent polyploidization in tumors after MDA treatment.

• The Korean Journal of Pharmacology
• /
• v.32 no.1
• /
• pp.39-49
• /
• 1996

In the present study, we observed change in intracellular $Ca^{2+}$$([Ca^{2+}]_i)$ as measured with the fluorescent $Ca^{2+}-indicator$ fura-2 in association with force development of the rat basilar arteries during activation by$K^+$ depolarizing solution and U46619, a thromboxane analogue, in the absence and the presence of calcitonin-gent related peptide (CGRP). CGRP (30 and 100 nM) caused a concentration-dependent inhibition of U46619-induced contraction with decrease in $[Ca^{2+}]_i$, whereas it did not exert any effect on the $K^+$ (90 mM)-induced contraction and increase in $[Ca^{2+}]_i$, Further, $[Ca^{2+}]_i-force$ relationships were determined by plotting the ratio of $F_{340}/F_{380}$ $([Ca^{2+}]_i)$ as a function of the force induced by U46619, and the results were compared with those obtained in the presence of CGRP. The curves obtained in the presence of CGRP (30 and 100 nM) were significantly moved to downward without right shift of the curves suggesting that CGRP inhibited the U46619-induced contraction only by mediation of reduction in $[Ca^{2+}]_i$ with out any change in the sensitivity of contractile apparatus to $Ca^{2+}$. The CGRP-induced attenuation of $[Ca^{2+}]_i$ and force development was significantly inhibited under pretreatment with CGRP $(8{\sim}37)$ fragment (100 nM), a CGRP1 receptor antagonist. Both the reduced contraction and reduction in $[Ca^{2+}]_i$ caused by CGRP were fully reversed by pretreatment with charybdotoxin (100 nM) and iberiotoxin (100 nM), large conductance $Ca^{2+}-activated$ $K^+$ channel blockers, but not by apamin (300 nM), a small conductance $Ca^{2+}-activated$ $K^+$ channel blocker, and glibenclamide ( 1 ${\mu}M$), an ATP-sensitive $K^+$ channel blocker. In conclusion, it is suggested that the CGRP1 receptor, upon activation by CGRP, are coupled to opening of $Ca^{2+}-activated$ $K^+$ channel and cause to decrease in $[Ca^{2+}]_i$, thereby leading to vasodilation of the rat basilar artery. However, it is not defined that the mechanism underlying vasodilation whether the $K^+$ channel blockers, charybdotoxin and iberiotoxin directly block the CGRP receptors and that CGRP-evoked relaxation is dependent on the cyclic AMP or $K^+$ channel opening or both actions.

• Biomolecules & Therapeutics
• /
• v.19 no.3
• /
• pp.288-295
• /
• 2011

Amyloid beta ($A{\beta}$)-induced neurotoxicity is a major pathological mechanism of Alzheimer's disease (AD). In this study, we investigated the inhibitory effect of L-theanine, a component of green tea (Camellia sinensis) on $A{\beta}_{1-42}$-induced neurotoxicity and oxidative damages of macromolecules. L-theanine inhibited $A{\beta}_{1-42}$-induced generation of reactive oxygen species, and activation of extracellular signal-regulated kinase and p38 mitogenic activated protein kinase as well as the activity of nuclear factor kappa-B. L-theanine also signifi cantly reduced oxidative protein and lipid damage, and elevated glutathione level. Consistent with the reduced neurotoxic signals, L-theanine (10-50 ${\mu}g$/ml) concomitantly attenuated $A{\beta}_{1-42}$ (5 ${\mu}M$)-induced neurotoxicity in SK-N-MC and SK-N-SH human neuroblastoma cells. These data indicate that L-theanine on $A{\beta}$-induced neurotoxicity prevented oxidative damages of neuronal cells, and may be useful in the prevention and treatment of neurodegenerative disease like AD.