• Journal of the Korean Chemical Society
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• v.42 no.2
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• pp.177-183
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• 1998

By the reactions of a $C_{2}$-chiral ligand, (+)-11S,12S-bis[2,2'-(diphenylphosphino)benzanilido]-9,10-dihydro-9,10-ethanoanthracene(6) with $[\pi-allyl chloroplatinum(II)]_4$, and $CpCo(CO)_2$ respectively, three new complexes, ($\pi$-allyl)platinum(II)(+)-11S,12S-bis[2,2'-(diphenylphosphino)benzanilido]-9,10-dihydro-9,10-ethanoanthracene perchlorate(1), ($\pi$-allyl)platinum(II)(+)-11S,12S-bis[2,2'-(diphenylphosphino)benzanilido]-9,10-dihydro-9,10-ethanoanthracene chloride(2), ($\eta^5$-cyclopentadienyl)cobalt(I)-(+)-11S,12S-bis[2,2'-(diphenylphosphino)benzanilido]-9,10-dihydro-9,10-ethanoanthracene(3) were prepared. $\eta^3$-Cyclohexenyl)palladium(II)1,2-bis(diphenylphosphino)ethane perchlorate(4) was obtained by the reaction of ($\eta^3$-cyclohexenyl)palladium(II) chloride dimer with a symmetric ligand, 1,2-bis(diphenylphosphino)ethane and lithium perchlorate. These complexes were identified by NMR-, IR-, and Mass-Spectrophotometers and elemental analyzer.

• Journal of the Korean Chemical Society
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• v.37 no.5
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• pp.543-546
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• 1993

• Biomedical Science Letters
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• v.27 no.2
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• pp.95-98
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• 2021

The S100 family proteins act as inducers of cancer cell apoptosis and inflammatory mediators. This study examined the pro-apoptotic mechanism caused by S100A8 and S100A9 in human FIP1L1-PDGFRα-positive eosinophilic leukemia cells. S100A8 and S100A9 elicited the death of EoL-1 cells in a time and dose-dependent manner. The activation of PDGFRα was suppressed by a decrease in PDGFRα after treatment with S100A8 and S100A9. Cycloheximide, a translation inhibitor, suppressed PDGFRα expression from 1 h to 5 h, and a co-treatment with S100A8 and S100A9 boosted the decrease in expression. The phosphorylation and expression of STAT5 decreased after treatment with S100A8 and S100A9 in EoL-1 and imatinib-resistant (EoL-1-IR) cells. S100A8 and S100A9 induced the chemotaxis of EoL-1 cells but did not affect the chemoattraction of EoL-1-IR. These findings indicate the cell death mechanism due to S100 family proteins and the development of leukemia therapy using S100A8 and S100A9.

• Applied Biological Chemistry
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• v.37 no.5
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• pp.402-408
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• 1994

For the examination of the role of monocerin(1) on the biological activity, (8S, 9S, 11R)-(-)-monocerin(20) and (9S, 11R)-(+)-fusarentin 4, 5-dimethyl ether(19) were synthesized by a condensation of the benzylic anion of ethyl 2, 3, 4-trimethoxy-6-methylbenzoate(16) with modifyed (R)-ethyl 3-hydroxyhexanoate (9). In a key step, bioreduction with active dried baker's yeast in organic solvent system was employed to get a chiral aldehyde 12. Their phytotoxic activities were tested on rice seedlings and lettuce seeds.

• Journal of Life Science
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• v.21 no.8
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• pp.1076-1082
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• 2011

Microtubule-based kinesin motor proteins are used for long-range vesicular transport. KIF5s (KIF5A, KIF5B and KIF5C) mediate the transport of various membranous vesicles along microtubules, but the mechanism behind how they recognize and bind to a specific cargo has not yet been completely elucidated. To identify the interaction protein for KIF5B, yeast two-hybrid screening was performed and a specific interaction with the unconventional myosin Myo9b, an actin-based vesicle transport motor, was found. The GTPase-activating protein (GAP) domain of Myo9s was essential for interaction with KIF5B in the yeast two-hybrid assay. Myo9b bound to the carboxyl-terminal region of KIF5B and to other KIF5 members. In addition, glutathione S-transferase (GST) pull-downs showed that Myo9s specifically interact to the complete Kinesin-I complex. An antibody to KIF5B specifically co-immunoprecipitated KIF5B associated with Myo9s from mouse brain extracts. These results suggest that kinesin-I motor protein interacts directly with actin-based motor proteins in the cell.

• Journal of the Korean Chemical Society
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• v.40 no.4
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• pp.219-228
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• 1996

An ab initio molecular orbital method has been applied to investigation of molecular properties and equilibrium geometries for hexahydroxybenzene triscarbonate (C9O9) and its analogous cyclic compounds (C9S9, C9O6S3, C9O3S6). In these works, the optimized geometry of each compound has been obtained at HF and MP2 levels. These results have shown that the optimized geometries of these compounds prefer D3h planar structure to C3v bowl structure. Calculations of harmonic vibrational frequencies have been also carried out at HF/3-21G* level to analyze normal modes of these compounds. Bonding characters of these compounds are studied by Mulliken and natural populations obtained at HF/6-31G* level. We have also studied the structures and the populations of C6O6 and C6S6 at HF and MP2 levels which are obtained by pyrolyses of C9O9 and analogous compounds. In addition, the single point calculations have been performed to predict the approximate energy barrier for pyrolysis of each compound.

• Korean Journal of Clinical Laboratory Science
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• v.40 no.1
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• pp.6-17
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• 2008

From the total 116,429 clinical specimens submitted to "C" hospital from January 2005 to December 2006, 2,195 strains of streptococci were isolated. Twenty four species of Streptococcus were identified with 0.1~19.8% isolation frequencies, of which S. pneumoniae was 19.8%, S. agalactiae 16.2%, S. anginosus 9.8%, S. constellatus 5.0%, S. oralis 3.9%, S. mitis 3.3%, S. pyogenes 2.7%, S. salivarius subsp. salivarius 2.2%, S. sanguinis 1.9%. For S. pneumoniae, clinical specimens showing over 9.0% isolation rate were 82.8% in sputum, 9.2% in blood, and for Streptococcus species other than S. pneumoniae, 18.0% in sputum, 16.0% in urine and 9.7% in blood. The antimicrobial agents that showed over 90.0% susceptibility were cefotaxime, gatilfloxacin, imipenem, levofloxacin, linezolid, moxifloxacin, rifampin and sporfloxacin in S. pneumoniae, ampicillin, cefotaxime, cetriaxone, levofloxacin, linezolid, penicillin, quinupristin/dalfopristin and vancomycin in S. agalactiae, chloramphenicol, clindamycin, levofloxacin and vancomycin in S. anginosus, levofloxacin, vancomycin in S. constellatus subsp. constellatus, vancomycin in S. oralis, vancomycin in S. mitis, chloramphenicol, clindamycin, levofloxacin, quinupristin/dalfopristin and vancomycin in S. pyogenes, chloramphenicol, levofloxacin and vancomycin in S. salivarius subsp. salivarius, chloramphenicol, levofloxacin and vancomycin in S. bovis II, chloramphenicol, levofloxacin, quinupristin/dalfopristin and vancomycin in S. dysgalactiae subsp. dysgalactiae, levofloxacin, chloramphenicol and vancomycin in the whole group of 10 Streptococcus spp. other than Streptococcus pneumoniae.

• Korean Journal of Clinical Laboratory Science
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• v.49 no.2
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• pp.128-134
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• 2017

Der p 1 and Der p 2 are essential allergens of house dust mite associated with the development of asthma. In the present study, we examined whether Der p 1 and Der p 2 induce a release of S100A8 and S100A9 in monocytes, which are involved in the regulatory mechanism of neutrophil apoptosis. We found that Der p 1 and Der p 2 significantly increased the secretion of S100A8 and S100A9 in normal monocytes. Moreover, S100A8 and S100A9 strongly suppressed the spontaneous apoptosis of normal and asthmatic neutrophils. The inhibitory effect of S100A9 was stronger than that of S100A8, and asthmatic neutrophils showed a higher inhibitory effect than normal neutrophils. S100A8 and S100A9 induced activation of Lyn, Akt, and ERK in a time-dependent manner. These findings elucidate the roles of Der p 1 and Der p 2 in the interaction between monocytes and neutrophils, as well as contributing to our knowledge of the pathogenesis of allergic diseases.

• Natural Product Sciences
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• v.10 no.3
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• pp.124-128
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• 2004

Previously, $(1R,9S)-{\beta}-Hydrastine$ hydrochloride has been found to lower dopamine content in PC12 cells (Kim et al., 20001). In this study, the effects of $(1R,9S)-{\beta}-Hydrastine$ hydrochloride on L-DOPA-induced cytotoxicity in PC12 cells were investigated. Treatment with $(1R,9S)-{\beta}-Hydrastine$ hydrochloride at concentrations higher than $500\;{\mu}M$ caused cytotoxicity in PC12 cells. In addition, $(1R,9S)-{\beta}-Hydrastine$ hydrochloride at non-cytotoxic or cytotoxic concentrations significantly enhanced L-DOPA-induced cytotoxicity (L-DOPA concentration, $50\;{\mu}M$). Treatment of PC12 cells with $750\;{\mu}M$ $-1R,9S)-{\beta}-Hydrastine$ hydrochloride and $50\;{\mu}M$ L-DOPA, alone or in combination, also induced cell death via a mechanism which exhibited morphological and biochemical characteristics of apoptosis, including chromatin condensation and membrane blebbing. Exposure of PC12 cells to $(1R,9S)-{\beta}-Hydrastine$ hydrochloride, L-DOPA and $(1R,9S)-{\beta}-Hydrastine$ hydrochloride plus L-DOPA for 48 h resulted in a marked increase in the cell loss and percentage of apoptotic cells compared with exposure for 24 h. These data indicate that $(1R,9S)-{\beta}-Hydrastine$hydrochloride at higher concentration ranges aggravates L-DOPA-induced neurotoxicity cytotoxicity in PC12 cells. Therefore, it is proposed that the long-term L-DOPA therapeutic patients with $(1R,9S)-{\beta}-Hydrastine$ hydrochloride could be checked for the adverse symptoms.

• Parasites, Hosts and Diseases
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• v.34 no.2
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• pp.135-142
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• 1996

Antigenic domain of jai or surface protein (p30) of Toxoplosmc Sondii was analyzed after polymerase chain reaction (PCR) of its gene fragments. Hydrophilic or hydrophobic moiety of amino acid sequences were expressed as glutathione S-transferase (G57) fusion proteins. Fragments of p30 gene were as follows: 737, total p30 open reading frame (ORF) ; S28, total ORF excluding N-terminal signal sequence and C-terminal hydrophobic sequence; Al9, N-terminal 2/3 parts of A28; A19, N-terminal 2/3 of S28; P9, C-terminal 2/3 part of S28; Z9. middle 1/3 of S28; and 29, C-terminal 1/3 of S28. respectively. Primer of each fragment was synthesized to include clamp sequence of EcoR I restriction site. PCR amplified DNA was inserted info GST (26 kDa) expression vector, PGEX-47-1 to transform into Escheri,hia coei (.JM105 strain). G57 fusion proteins were expressed with IPTG induction as 63. 54, 45, 45, 35, 36. and 35 kDa proteins measured by SDS-PAGE. Each fusion protein was confirmed with G57 detection kit. Western blot analysis with the serum of a toxoplasmosis patient revealed antigenicity in proteins expressed by T37. S28, and Al9 but not those by Pl8. X9, Y10, and Z9. Antigenicity of p30 seems to be located either in N-terminal 115 part in the presence of middle 1/3 part or in the oligopeptides between margins of the first and second 1/3 parts.