• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2002.08a
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• pp.84-91
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• 2002

The stochiometric composition of $AgGaS_2$/GaAs polycrystal source materials for the $AgGaS_2$/GaAs epilayer was prepared from horizontal furnace. From the extrapolation method of X-ray diffraction patterns it was found that the polycrystal $AgGaS_2$/GaAs has tetragonal structure of which lattice constant an and Co were 5.756 $\AA$ and 10.305 $\AA$, respectively. $AgGaS_2$/GaAs epilayer was deposited on throughly etched GaAs(100) substrate from mixed crystal $AgGaS_2$/GaAs by the Hot Wall Epitaxy (HWE) system. The source and substrate temperature were $590^{\circ}C$ and $440^{\circ}C$ respectively. The crystallinity of the grown $AgGaS_2$/GaAs epilayer was investigated by the DCRC (double crystal X-ray diffraction rocking curve). The optical energy gaps were found to be 2.61 eV for $AgGaS_2$/GaAs epilayer at room temperature. The temperature dependence of the photocurrent peak energy is well explained by the Varshni equation, then the constants in the Varshni equation are given by $\alpha=8.695{\times}10^{-4}$ eV/K, and $\beta=332K$. From the photocurrent spectra by illumination of polarized light of the $AgGaS_2$/GaAs epilayer, we have found that crystal field splitting ${\Delta}Cr$ was 0.28 eV at 20 K. From the PL spectra at 20 K, the peaks corresponding to free and bound excitons and a broad emission band due to D-A pairs are identified. The binding energy of the free excitons are determined to be 0.2676 eV and 0.2430 eV and the dissociation energy of the bound excitons to be 0.4695 eV.

• Korean Journal of Materials Research
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• v.9 no.3
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• pp.327-332
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• 1999

The recovery activation energy, the order of reaction and the recovery rate constant were detemined by isochronal and isothermal annealing treatment to investigate the recovery behaviors of neutron irradiated Mn-Mo-Ni low alloy steels$(fluence: 2.3\times10^{19}ncm^{-2}, 553K, E\geq1.0 MeV)$. Vickers microhardness tests were conducted to trace the recovery behavior after heat treatments. The results were analyzed in terms of recovery stages, behavior of responsible defects and recovery kinetics. It was shown that recovery occurred through two annealing stages(stage I : 703-753K, stage n : 813-873K) with re$\infty$very activation energies of 2.5 eV and 2.93 eV for each stage I and n, respectively. From the comparison of unirradiated and irradiated isochronal anneal curves, a radiation anneal hardening(RAH) peak was identified at around 813K. Most of recovery have occurred during about 120 min irrespective of isothermal annealing temperatures of 743K and 833K. Recovery rate constants were determined to be $3.4\times10^{-4}min^{-1} and 7.1\times10^{-4}min^{-1}$ for stage I and II, respectively. The order of reaction was about 2 for both recovery stages. Comparing the obtained data with those of previously reported results on neutron irradiated Mn- Mo- Ni steels, the thermal recovery be­havior of the present material seems to occur by the dissociation of point defect clusters formed during irradiation, and by the recombination process of self-interstitials and vacancies from dissociated vacancy clusters.

• Biomolecules & Therapeutics
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• v.3 no.4
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• pp.266-272
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• 1995

The analysis of membrane receptors for hormones and neurotransmitters has progressed considerably by pharmacological and biochemical means and more recently through the use of specific antibodies. To generate and characterize a moloclonal antibody against $\beta$-adrenergic receptor, a synthetic $\beta$2-adrenergic receptor peptide (Phe-Gly-Asn-Phe-Trp-Cys-Phe-Trp-Thr-Ser-lle-Asp-Val-Leu) which may comprise part of $\beta$-adrenergic receptor ligand binding pocket was coupled to Keyhole Limpet Hemocyanin (KLH) and used as an immunogen. Male BALB/C mice were immunized with this antigen and the immunized spleen was fused with myeloma SP2/0-Ag14 cells to produce monoclonal antibodies. Two clones were obtained but one of monoclonal antibodies, mAb5G09, was used throughout in this study because the other clone, mAb5All showed weak immunoreactivity against KLH as well. The mouse monoclonal antibody mAb5G09 produced in this study showed immunoreactivity to peptide-KLH conjugates and also to human A43l cells and guinea pig lung $\beta$2-adrenergic receptor as revealed by ELISA and western blot. In the course of determination of the effects of mAb5G09 on $\beta$-receptor ligand binding, it was observed that mAb5G09 specifically bound $\beta$-adrenergic radioligand [$^3$H]dihydroalprenolol (DHA) with a dissociation constant (Kd) of 60 nM. The [$^3$H]DHA binding activity of mAb5G09 had characteristics of immunoglobulins and the binding activity was not observed in the control anti-KLH monoclonal antibody. The monoclonal antibody, mAb5G09 produced in this study may provide useful models for the study of the structure of receptor binding sites.

• Molecules and Cells
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• v.44 no.1
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• pp.26-37
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• 2021

Human papillomaviruses (HPVs) cause cellular hyperproliferation-associated abnormalities including cervical cancer. The HPV genome encodes two major viral oncoproteins, E6 and E7, which recruit various host proteins by direct interaction for proteasomal degradation. Recently, we reported the structure of HPV18 E7 conserved region 3 (CR3) bound to the protein tyrosine phosphatase (PTP) domain of PTPN14, a well-defined tumor suppressor, and found that this intermolecular interaction plays a key role in E7-driven transformation and tumorigenesis. In this study, we carried out a molecular analysis of the interaction between CR3 of HPV18 E7 and the PTP domain of PTPN21, a PTP protein that shares high sequence homology with PTPN14 but is putatively oncogenic rather than tumor-suppressive. Through the combined use of biochemical tools, we verified that HPV18 E7 and PTPN21 form a 2:2 complex, with a dissociation constant of 5 nM and a nearly identical binding manner with the HPV18 E7 and PTPN14 complex. Nevertheless, despite the structural similarities, the biological consequences of the E7 interaction were found to differ between the two PTP proteins. Unlike PTPN14, PTPN21 did not appear to be subjected to proteasomal degradation in HPV18-positive HeLa cervical cancer cells. Moreover, knockdown of PTPN21 led to retardation of the migration/invasion of HeLa cells and HPV18 E7-expressing HaCaT keratinocytes, which reflects its protumor activity. In conclusion, the associations of the viral oncoprotein E7 with PTPN14 and PTPN21 are similar at the molecular level but play different physiological roles.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.48 no.4
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• pp.321-330
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• 2022

This study attempted to establish an optimal multi-compound simultaneous analysis method that can secure reliable results for 15 - preservatives, 2 - sun screens and 1 - antioxidants of cosmetics using HPLC-PDA. Since the potential of hydrogen (pH) in the mobile phase affects the acid dissociation constant (pKa) of the preservatives, and the peak retention time shift and area change were observed. The peak separation condition was established by adjusting the pH to 0.1% H₃PO₄ addition (mL) when preparing the mobile phase. As a results of method validation, the linearity correlation coefficient (R²) of above 0.999 were obtained, and accuracy 87.9 ~ 101.1%, 0.1 ~ 7.6% precision for two types of cosmetics (cream and shampoo). It was found that the limit of detection (LOD) was 0.1 ~ 0.2 mg/kg and the limit of quantitation (LOQ) was 2.0 ~ 4.0 mg/kg. In addition, it was possible to simultaneously separate p-anisic acid, a natural compound that was difficult to separate in HPLC due to the small difference from methylparaben, a synthetic preservatives. Through this study, it will be effectively used to secure quality control and safety for compound that need restrictions on use cosmetics.

• Journal of Ginseng Research
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• v.47 no.6
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• pp.743-754
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• 2023

Background: Myocardial fibrosis post-myocardial infarction (MI) can induce maladaptive cardiac remodeling as well as heart failure. Although 20(S)-ginsenoside Rg3 (Rg3) has been applied to cardiovascular diseases, its efficacy and specific molecular mechanism in myocardial fibrosis are largely unknown. Herein, we aimed to explore whether TGFBR1 signaling was involved in Rg3's anti-fibrotic effect post-MI. Methods: Left anterior descending (LAD) coronary artery ligation-induced MI mice and TGF-β1-stimulated primary cardiac fibroblasts (CFs) were adopted. Echocardiography, hematoxlin-eosin and Masson staining, Western-blot and immunohistochemistry, CCK8 and Edu were used to study the effects of Rg3 on myocardial fibrosis and TGFBR1 signaling. The combination mechanism of Rg3 and TGFBR1 was explored by surface plasmon resonance imaging (SPRi). Moreover, myocardial Tgfbr1-deficient mice and TGFBR1 adenovirus were adopted to confirm the pharmacological mechanism of Rg3. Results: In vivo experiments, Rg3 ameliorated myocardial fibrosis and hypertrophy and enhanced cardiac function. Rg3-TGFBR1 had the 1.78×10^-7 M equilibrium dissociation constant based on SPRi analysis, and Rg3 inhibited the activation of TGFBR1/Smads signaling dose-dependently. Cardiac-specific Tgfbr1 knockdown abolished Rg3's protection against myocardial fibrosis post-MI. In addition, Rg3 downregulated the TGF-β1-mediated CFs growth together with collagen production in vitro through TGFBR1 signaling. Moreover, TGFBR1 adenovirus partially blocked the inhibitory effect of Rg3. Conclusion: Rg3 improves myocardial fibrosis and cardiac function through suppressing CFs proliferation along with collagen deposition by inactivation of TGFBR1 pathway.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.10a
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• pp.34-63
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• 2003

Occupational and environmental exposure to manganese continue to represent a realistic public health problem in both developed and developing countries. Increased utility of MMT as a replacement for lead in gasoline creates a new source of environmental exposure to manganese. It is, therefore, imperative that further attention be directed at molecular neurotoxicology of manganese. A Need for a more complete understanding of manganese functions both in health and disease, and for a better defined role of manganese in iron metabolism is well substantiated. The in-depth studies in this area should provide novel information on the potential public health risk associated with manganese exposure. It will also explore novel mechanism(s) of manganese-induced neurotoxicity from the angle of Mn-Fe interaction at both systemic and cellular levels. More importantly, the result of these studies will offer clues to the etiology of IPD and its associated abnormal iron and energy metabolism. To achieve these goals, however, a number of outstanding questions remain to be resolved. First, one must understand what species of manganese in the biological matrices plays critical role in the induction of neurotoxicity, Mn(II) or Mn(III)? In our own studies with aconitase, Cpx-I, and Cpx-II, manganese was added to the buffers as the divalent salt, i.e., $MnCl_2$. While it is quite reasonable to suggest that the effect on aconitase and/or Cpx-I activites was associated with the divalent species of manganese, the experimental design does not preclude the possibility that a manganese species of higher oxidation state, such as Mn(III), is required for the induction of these effects. The ionic radius of Mn(III) is 65 ppm, which is similar to the ionic size to Fe(III) (65 ppm at the high spin state) in aconitase (Nieboer and Fletcher, 1996; Sneed et al., 1953). Thus it is plausible that the higher oxidation state of manganese optimally fits into the geometric space of aconitase, serving as the active species in this enzymatic reaction. In the current literature, most of the studies on manganese toxicity have used Mn(II) as $MnCl_2$ rather than Mn(III). The obvious advantage of Mn(II) is its good water solubility, which allows effortless preparation in either in vivo or in vitro investigation, whereas almost all of the Mn(III) salt products on the comparison between two valent manganese species nearly infeasible. Thus a more intimate collaboration with physiochemists to develop a better way to study Mn(III) species in biological matrices is pressingly needed. Second, In spite of the special affinity of manganese for mitochondria and its similar chemical properties to iron, there is a sound reason to postulate that manganese may act as an iron surrogate in certain iron-requiring enzymes. It is, therefore, imperative to design the physiochemical studies to determine whether manganese can indeed exchange with iron in proteins, and to understand how manganese interacts with tertiary structure of proteins. The studies on binding properties (such as affinity constant, dissociation parameter, etc.) of manganese and iron to key enzymes associated with iron and energy regulation would add additional information to our knowledge of Mn-Fe neurotoxicity. Third, manganese exposure, either in vivo or in vitro, promotes cellular overload of iron. It is still unclear, however, how exactly manganese interacts with cellular iron regulatory processes and what is the mechanism underlying this cellular iron overload. As discussed above, the binding of IRP-I to TfR mRNA leads to the expression of TfR, thereby increasing cellular iron uptake. The sequence encoding TfR mRNA, in particular IRE fragments, has been well-documented in literature. It is therefore possible to use molecular technique to elaborate whether manganese cytotoxicity influences the mRNA expression of iron regulatory proteins and how manganese exposure alters the binding activity of IPRs to TfR mRNA. Finally, the current manganese investigation has largely focused on the issues ranging from disposition/toxicity study to the characterization of clinical symptoms. Much less has been done regarding the risk assessment of environmenta/occupational exposure. One of the unsolved, pressing puzzles is the lack of reliable biomarker(s) for manganese-induced neurologic lesions in long-term, low-level exposure situation. Lack of such a diagnostic means renders it impossible to assess the human health risk and long-term social impact associated with potentially elevated manganese in environment. The biochemical interaction between manganese and iron, particularly the ensuing subtle changes of certain relevant proteins, provides the opportunity to identify and develop such a specific biomarker for manganese-induced neuronal damage. By learning the molecular mechanism of cytotoxicity, one will be able to find a better way for prediction and treatment of manganese-initiated neurodegenerative diseases.