• Journal of the Korean Chemical Society
• /
• v.39 no.5
• /
• pp.364-370
• /
• 1995

The catalytic oxidations of several olefins in $CH_2Cl_2$ have been investigated using non-redox metalloporphyrin (M=Ga(III), In(III), Tl(III)) complexes as catalyst and sodium hypochlorite as terminal oxidant. Porphyrins were $(p-CH_3O)TPP,\;(p-CH_3)TPP,\;TPP,\;(p-F)TPP,\;(p-Cl)TPP\;and\;(F_20)TPP$ (TPP=tetraphenylporphyrin), and olefins were $(p-CH_3O)-,\;(p-CH_3)-,\;(p-H)-,\;(p-F)-,\;(p-Cl)-\;and\;(p-Br)styrene$styrene and cyclopentene and cyclohexene. The substrate conversion yield was discussed according to the substituent effects of metalloporphyrin and substrate, and the radius effect of non-redox metal ion. The conversion yield of substrate by changing the substituent of TPP increased in the order of $p-CH_3O$ < $p-CH_3$ < H < p-F < p-Cl, which was consistent with the sequence of $4{\sigma}$ values of TPP. But the substituent effect of substrate on the conversion yield decreased with increasing the ${\sigma}^+$ values on substrates in the order of p-CH3O > p-CH3 > H > p-Cl > p-Br. For the oxidation of several olefins, the complexes of In(III)- and Tl(III)-porphyrins turned out to be more active catalysts than Ga(III)-porphyrin.

• Journal of Periodontal and Implant Science
• /
• v.32 no.4
• /
• pp.865-873
• /
• 2002

The primary cause of tooth loss after 30 years of age is periodontal disease. Destruction of alveolar bone by periodontal disease is done by bone resorbing activity of osteoclasts. Understanding differentiation and activation mechanism of osteoclasts is essential for controling periodontal disease. The purpose of this study is to identify the possible effects of Vitamin D and cytokines affecting osteoclasts and its precursor cells. Four to six week-old mice were killed and humerus, radius, tibia and femur were removed aseptically and washed two times with Hank's solution containing penicillin-streptomycin and then soft tissue were removed. Bone marrow cells were collected by 22 gauge needle. Cells were cultured in Hank's solution containing 1 mg/ml type II collagenase, 0.05% trypsin, 41mM EDTA. Supernatant solution was removed 5 times after 15 minutes of digestion with above mentioned enzyme solution, and remained bone particles were maintained in alpha-MEM for 15 minutes and $4^{\circ}C$ temperature. Bone particles were agitated for 1 minute and supernatant solution containing osteoclast precursor cells were filtrated with cell stainer. These separated osteoclast precursor cells were dispensed with 100-mm culture dish by $1{\times}10^7$ cells unit and cultured in ${\alpha}$- MEM containing 20 ng/ml recombinant human M-CSF, 30 ng/ml recombinant human soluble osteoclast differentiation factor and 10% fetal calf serum for 2 and 7 days. Total RNA of osteoclast precursor cells were extracted using RNeasy kit. One ${\mu}g$ of total RNA was reverse transcribed in $42^{\circ}C$ for 30 minutes using SuperScriptII reverse transcriptase. Expression of transcribed receptors of each hormone and cytokine were traced with 1 ${\mu}l$ of cDNA solution by PCR amplification. Vitamin D receptor WAS found in cells cultured for 7 days. TNF-${\alpha}$ receptor was found in cells cultured for 2 days and amount of receptors were increased by 7 days. IL-1 type I receptor was not found in cells cultured 2 and 7 days. But, IL-1 receptor type II was found in cells cultured for 2 days. TGF-${\alpha},{\beta}$type I receptor was found in cells cultured 2 and 7 days, and amount of receptors were increased by 7 days of culture. These results implies Vitamin D and cytokines can affect osteoclasts directly, and affecting period in differentiation cycle of osteoclasts is different by Vitamin D and cytokines.

• The Journal of Korean Institute of Electromagnetic Engineering and Science
• /
• v.29 no.11
• /
• pp.821-827
• /
• 2018

In devices used for re-forming osteoblasts to treat osteoporosis, a magnetic field is applied from the outside of the bone, and the minerals contained in the bone are aligned in a certain direction and undergo precessional motion. When a $90^{\circ}$ RF pulse is applied by using an RF coil, protons of minerals are brought to an excited state, and phosphorus activity promoting the deposition of osteoblasts in the bone is increased, thereby reshaping the bone. Miniaturizing the RF coil that generates a signal corresponding to the harmonic of the precessional motional frequency by means of the $90^{\circ}$ RF pulse can drastically reduce the overall size of the bone reshaping system. In this study, we propose a methodology for the miniaturization of the RF coil that can be used for osteoblast re-formation using a bone reshaping system. The capacitance of the designed RF coil is 25 pF, the inductance is approximately 100 nH, and the resonance frequency is 96 MHz. The radius of the end ring of the designed RF coil is 18 cm, and the total length of the leg is $2{\times}11.6cm$. The performance of the coil is verified through post-design measurement.

• Journal of Korean Tunnelling and Underground Space Association
• /
• v.24 no.2
• /
• pp.171-182
• /
• 2022

InSAR (Interferometry SAR) technique is a technique that uses complex data to obtain phase difference information from two or more SAR image data, and enables high-resolution image extraction, surface change detection, elevation measurement, and glacial change observation. In many countries, research on the InSAR technique is being conducted in various fields of study such as volcanic activity detection, glacier observation in Antarctica, and ground subsidence analysis. In this study, a case of large ground settlement due to groundwater level drawdown during tunnelling was introduced, and ground settlement analyses using InSAR technique and numerical analysis method were compared. The maximum settlement and influence radius estimated by the InSAR technique and numerical method were found to be quite similar, which confirms the reliability of the InSAR technique. Through this case study, it was found that the InSAR technique reliable to use for estimating ground settlement and can be used as a key technology to identify the long-term ground settlement history in the absence of measurement data.

• Journal of Environmental Health Sciences
• /
• v.48 no.6
• /
• pp.298-305
• /
• 2022

Background: The concentration of air pollutants as measured by the Air Quality Monitoring System (AQMS) is not an accurate population exposure level since actual human activities and temporal and spatial variability need to be considered. Therefore, to increase the accuracy of exposure assessment, the population should be considered. However, it is difficult to obtain population data due to limitations such as personal information. Objectives: The existing population defined in this study is the number of people in each region's grid. The purpose is to provide a methodology for evaluating exposure to PM_2.5 through existing population data provided by the National Geographic Information Institute. Methods: The selected study period was from October 26 to October 28, 2021. Using PM_2.5 concentration data measured at the Sensor-based Air Monitoring Station (SAMS) installed in Guro-gu and Wonju-si, the concentration for each grid was estimated by applying inverse distance weights through QGIS version 3.22. Considering the existing population, population-weighted average concentration (PWAC) was calculated and the exposure level of the population was compared by region. Results: The outdoor PM_2.5 concentration as measured through the SAMS was high in Wonju-si on all three days. Wonju-si showed an average 22% higher PWAC than Guro-gu. As a result of comparing the PWAC and outdoor PM_2.5 concentration by region, the PWAC in Guro-gu was 1~2% higher than the observed value, but it was almost the same. Conversely, observations of Wonju-si were 10.1%, 11.3%, and 8.2% higher than PWAC. Conclusions: It is expected that the Geographic Information System (GIS) method and the existing population will be used to evaluate the exposure level of a population with a narrow activity radius in further research. In addition, based on this study, it is judged that research on exposure to environmental pollutants and risk assessment methods should be expanded.

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