• Journal of the Korean Magnetic Resonance Society
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• v.5 no.2
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• pp.99-109
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• 2001

Authors investigated neuronal changes of local cellular metabolism in the cerebral lesions of Parkinsonian symptomatic side between before and after stereotactic neurosurgery by follow-up 1H magnetic resonance spectroscopy (MRS). Patients with Parkinson's disease (PD) (n = 15) and age-matched normal controls (n = 15) underwen MRS examinations using a stimulated echo acquisition mode (STEAM) pulse sequence that provided 2${\times}$2${\times}$2 ㎤ (8ml) volume of interest in the regions of substantia nigra, thalamus, and lentiform nucleus. Spectral parameters were 20 ms TE, 2000 ms TR, 128 averages,2500 Hz spectral width, and 2048 data points. Raw data were processed by the SAGE data analysis package (GE Medical Systems). Peak areas of N-acetylaspartate (NAA), creatine (Cr), choline-containing compounds (Cho), inositols (Ins), and the sum (Glx) of glutamate and GABA were calculated by means of fitting the spectrum to a summation of Lorentzian curves using Marquardt algorithm. After blindly processed, we evaluated neuronal alterations of observable metabolite ratios between before and after stereotactic neurosurgery using Pearson product-moment analysis (SPSS, Ver. 6.0). A significant reduction of NAA/Cho ratio was observed in the cerebral lesion in substantia nigra of PD patient related to the symptomatic side after neurosurgery (P : 0.03). In thalamus, NAA/Cho ratio was also significantly decreased in the cerebral lesion including the electrode-surgical region (P : 0.03). A significant reduction of NAA/Cho ratio in lentiform nucleus was not oberved, but tended toward significant reduction after neurosurgery (P = 0.08). In particular, remarkable lactate signal was noted from the surgical thalamic lesions of 6 among 8 patients and internal segments of globus pallidus of 6 among 7 patients, respectively. Significant metabolic alterations of NAA/Cho ratio might reflect functional changes of neuropathological processes in the lesion of substantia nigra, thalamus, and lentiform nucleus, and could be a valuable finding fur evaluation of Parkinson's disease after neurosurgery. Increase of lactate signals, being remarkable in surgical lesions, could be consistent with a common consequence of neurosurgical necrosis. Thus, IH MRS could be a useful modality to evaluate the diagnostic and prognostic implications fur Parkinsons disease after functional neurosurgery.

• Proceedings of the Microbiological Society of Korea Conference
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• 2007.05a
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• pp.120-122
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• 2007

All living organisms use numerous signal-transduction pathways to sense and respond to their environments and thereby survive and proliferate in a range of biological niches. Molecular dissection of these signalling networks has increased our understanding of these communication processes and provides a platform for therapeutic intervention when these pathways malfunction in disease states, including infection. Owing to the expanding availability of sequenced genomes, a wealth of genetic and molecular tools and the conservation of signalling networks, members of the fungal kingdom serve as excellent model systems for more complex, multicellular organisms. Here, we employed Cryptococcus neoformans as a model system to understand how fungal-signalling circuits operate at the molecular level to sense and respond to a plethora of environmental stresses, including osmoticshock, UV, high temperature, oxidative stress and toxic drugs/metabolites. The stress-activated p38/Hog1 MAPK pathway is structurally conserved in many organisms as diverse as yeast and mammals, but its regulation is uniquely specialized in a majority of clinical Cryptococcus neoformans serotype A and D strains to control differentiation and virulence factor regulation. C. neoformans Hog1 MAPK is controlled by Pbs2 MAPK kinase (MAPKK). The Pbs2-Hog1 MAPK cascade is controlled by the fungal "two-component" system that is composed of a response regulator, Ssk1, and multiple sensor kinases, including two-component.like (Tco) 1 and Tco2. Tco1 and Tco2 play shared and distinct roles in stress responses and drug sensitivity through the Hog1 MAPK system. Furthermore, each sensor kinase mediates unique cellular functions for virulence and morphological differentiation. We also identified and characterized the Ssk2 MAPKKK upstream of the MAPKK Pbs2 and the MAPK Hog1 in C. neoformans. The SSK2 gene was identified as a potential component responsible for differential Hog1 regulation between the serotype D sibling f1 strains B3501 and B3502 through comparative analysis of their meiotic map with the meiotic segregation of Hog1-dependent sensitivity to the fungicide fludioxonil. Ssk2 is the only polymorphic component in the Hog1 MAPK module, including two coding sequence changes between the SSK2 alleles in B3501 and B3502 strains. To further support this finding, the SSK2 allele exchange completely swapped Hog1-related phenotypes between B3501 and B3502 strains. In the serotype A strain H99, disruption of the SSK2 gene dramatically enhanced capsule biosynthesis and mating efficiency, similar to pbs2 and hog1 mutations. Furthermore, ssk2, pbs2, and hog1 mutants are all hypersensitive to a variety of stresses and completely resistant to fludioxonil. Taken together, these findings indicate that Ssk2 is the critical interface protein connecting the two-component system and the Pbs2-Hog1 pathway in C. neoformans.

• The Journal of Korean Institute of Communications and Information Sciences
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• v.31 no.5B
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• pp.456-477
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• 2006

Due to advances in wireless communication technology and increasing demand for various types of wireless access, cellular, WLAN, and portable internet(such as WiBro and IEEE 802.16) systems are likely to be integrated into a unified wireless access system. This expectation premises the availability of multi-mode handsets and cooperative interworking of heterogenous wireless access networks allied by roaming contracts. Under such environments, a user may lie in the situation where more than one wireless accesses are available at his/her location, and he/she will want to choose the 'best' access among them. In this paper, we define the 'best' access(es) as the access(es) that charges minimum cost while fulfilling the required QoS of wireless access, and address the problem of choosing the optimal set of accesses theoretically by introducing a graph representation of service environment. Two optimal selection algorithms are proposed, which individually consider cases where single or multiple wireless access can be supported by multi-mode handsets.

• Journal of Korean Physical Therapy Science
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• v.13 no.2
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• pp.99-119
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• 2006

Endothelin (ET) is a 21 amino acid peptide with multifunctional effects on the vasculature as well as a variety of other cell types such as respiratory, gastrointestinal, urogenital, endocrine, central nervous systems, and others. Endothelin has emerged as a modulator by autocrine and paracrine actions for many cellular activities, including vasoconstriction, cell proliferation, hormone production, neurotransmitter and/or neuromodulator. The endothelin family consists of three closely related peptides, ET-1, ET-2, and ET-3 derived from separate genes, such as chromosome 6, 1, and 20, respectively. ET-1 is the predominant isoform produced in the cardiovascular system and about which most is known. Endothelin receptors are seven-transmembrane GTP-binding protein-coupled receptors, which are classified into endothelin-A (ETA) and endothelin-B (ETB) receptors. Interestingly, recent evidence is accumulating to suggest that ET -1 may contribute to a variety of pain states such as allodynia and hyperalgesia in animals and humans. Therefore, in this review the biological characteristics and contraction-related mechanism of endothelin-1 in mammalian cells will be summarized. Especially, we focus on multifunctional roles for ET-1 in noxious stimulation-induced pain for the study of pain specialized physical therapy.

• Molecules and Cells
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• v.25 no.4
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• pp.467-478
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• 2008

Simple sequence repeats (SSRs) and interSSR (ISSR) marker systems were used in this study to reveal genetic changes induced by artificial selection for short/long larval duration in the tropical strain Nistari of the silkworm Bombyx mori. Artificial selection separated longer larval duration (LLD) ($29.428{\pm}0.723days$) and shorter larval duration (SLD) ($22.573{\pm}0.839days$) lines from a base, inbred population of Nistari (larval span of $23.143{\pm}0.35days$). SSR polymorphism was observed between the LLD and SLD lines at one microsatellite locus, Bmsat106 ($CA_7$) and at two loci of 1074 bp and 823 bp generated with the ISSR primer UBC873. Each of these loci was present only in the LLD line. The loci segregated in the third generation of selection and were fixed in opposite directions. In the $F_2$ generation of the $LLD{\times}SLD$ lines, the alleles of Bmsat106 and $UBC873_{1074bp}$ segregated in a 1:1 ratio and the loci were present only in the LLD individuals. $UBC873_{823bp}$ was homozygous. Single factor ANOVA showed a significant association between the segregating loci and longer larval duration. Together, the two alleles contributed to an 18% increase in larval duration. The nucleotide sequences of the $UBC873_{1074bp}$ and $UBC873_{823bp}$ loci had 67% A/T content and consisted of direct, reverse, complementary and palindromic repeats. The repeats appeared to be "nested" (59%) in larger repeats or as clustered elements adjacent to other repeats. Of 203 microsatellites identified, dinucleotides (67.8%) predominated and were rich in A/T and T/A motifs. The sequences of the $UBC873_{1074bp}$ and $UBC873_{823bp}$ loci showed similarity (E = 0.0) to contigs located in Scaffold 010774 and Scaffold 000139, respectively, of the B. mori genome. BLASTN analysis of the $UBC873_{1074bp}$ sequence showed significant homology of (nt.) 45-122 with upstream region of three exons from Bombyx. The complete sequence of this locus showed ~49% nucleotide conservation with transposon 412 of Drosophila melanogaster and the Ikirara insertions of Anopheles gambiae. The A + T richness and lack of coding potential of these small loci, and their absence in the SLD line, reflect the active process of genetic change associated with the switch to short larval duration as an adaptation to the tropics.

• Molecular & Cellular Toxicology
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• v.4 no.4
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• pp.348-354
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• 2008

Bisphenol A (BPA), an environmental endocrine disrupter, enters the human body continuously in food and drink. Young children are likely to be more vulnerable than adults to chemical exposure due to the immaturities of their organ systems, rapid physical development, and higher ventilation, metabolic rates, and activity levels. The direct effect of BPA on peripheral tissue might also be of importance to the development of insulin resistance. However, the influence that BPA has on insulin signaling molecules in skeletal muscle has not been previously investigated. In this study, we examined the effect of BPA on fasting blood glucose (FBG) in post-weaned Wistar rats and on insulin signaling proteins in C2C12 skeletal muscle cells. Subsequently, we investigated the effects of BPA on insulin-mediated Akt phosphorylation in C2C12 myotubes. In rats, BPA treatment (0.1-1,000 ng/mL for 24 hours) resulted in the increase of FBG and plasma insulin levels, and reduced insulin-mediated Akt phosphorylation. Furthermore, the mRNA expression of insulin receptor (IR) was decreased after 24 hours of BPA treatment in C2C12 cells in a dose-dependent manner, whereas the mRNA levels of other insulin signaling proteins, including insulin receptor substrate-1 (IRS-1) and 5'-AMP-dependent protein kinase (AMPK), were unaffected. Treatment with BPA increased GLUT4 expression and protein tyrosine phosphatase 1B (PTP1B) activity in C2C12 myotubes, but not in protein levels. We conclude that exposure to BPA can induce insulin resistance by decreasing IR gene expression, which is followed by a decrease in insulin- mediated Akt activation and increased PTP1B activity.

• Proceedings of the Microbiological Society of Korea Conference
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• 2008.05a
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• pp.42-44
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• 2008

Bacterial biofilms are analogous to multi-cellular organisms or to clonal communities of higher organisms. In this respect, it can be demonstrated that biofilms display the type of genetic variation associated with macroorganisms. The formation of genetic variants from biofilms is the result of internally produced and regulated signals and the appearance of these variants coincides with dispersal from the biofilm. Moreover, the generation of such variation, has similar outcomes for the bacterial community, where diversification of phenotypic traits ensures that the bacterial community optimizes its chances of success when dispersing or surviving when challenged with environmental stress. These observations increase the complexity with which we view bacteria and also suggest that microbial systems can serve as models for the testing of eukaryotic ecological theories.

• Proceedings of the Materials Research Society of Korea Conference
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• 2012.05a
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• pp.72-72
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• 2012

Lithium rechargeable batteries have been widely used as key power sources for portable devices for the last couple of decades. Their high energy density and power have allowed the proliferation of ever more complex portable devices such as cellular phones, laptops and PDA's. For larger scale applications, such as batteries in plug-in hybrid electric vehicles (PHEV) or power tools, higher standards of the battery, especially in term of the rate (power) capability and energy density, are required. In PHEV, the materials in the rechargeable battery must be able to charge and discharge (power capability) with sufficient speed to take advantage of regenerative braking and give the desirable power to accelerate the car. The driving mileage of the electric car is simply a function of the energy density of the batteries. Since the successful launch of recent Ni-MH (Nickel Metal Hydride)-based HEVs (Hybrid Electric Vehicles) in the market, there has been intense demand for the high power-capable Li battery with higher energy density and reduced cost to make HEV vehicles more efficient and reduce emissions. However, current Li rechargeable battery technology has to improve significantly to meet the requirements for HEV applications not to mention PHEV. In an effort to design and develop an advanced electrode material with high power and energy for Li rechargeable batteries, we approached to this in two different length scales - Atomic and Nano engineering of materials. In the atomic design of electrode materials, we have combined theoretical investigation using ab initio calculations with experimental realization. Based on fundamental understanding on Li diffusion, polaronic conduction, operating potential, electronic structure and atomic bonding nature of electrode materials by theoretical calculations, we could identify and define the problems of existing electrode materials, suggest possible strategy and experimentally improve the electrochemical property. This approach often leads to a design of completely new compounds with new crystal structures. In this seminar, I will talk about two examples of electrode material study under this approach; $LiNi_{0.5}Mn_{0.5}O_2$ based layered materials and olivine based multi-component systems. In the other scale of approach; nano engineering; the morphology of electrode materials are controlled in nano scales to explore new electrochemical properties arising from the limited length scales and nano scale electrode architecture. Power, energy and cycle stability are demonstrated to be sensitively affected by electrode architecture in nano scales. This part of story will be only given summarized in the talk.

• Advances in Traditional Medicine
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• v.5 no.3
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• pp.216-230
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• 2005

Although the field of study in immune enhancing compounds is relatively new, natural products from plants represent a rich and promising source of novel molecules with immunomodulating properties, Microglial cells, the main immune effector cells of the brain, usually display a ramified morphology and low expression levels of immunologically relevant antigens such as MHC class I and class II. Since any compound which participates in activation of phagocytic cells contributes to the production of potentially toxic factors, the search for convenient in vitro test-systems and study of mechanisms of action of these agents are of great interest. Human blood polymorphonuclear (PMN) cells and primary microglial cells isolated from Sprague-Dawley rats were used as cellular screening tests for study of phagocytosis-stimulating action of immunomodulating agents. Numbers of phagocytic activity were evaluated by the phagocyte ingestion of yeast cells and NO-synthase activity, nitrite production, and nitroblue tetrazolium test were determined after phagocyte stimulation. It was possible to demonstrate that indexes of phagocytic activity can be used as quantitative indicators for measurement immunomodulating activity. As a positive control, Zymosan A-induced phagocytosis in both PMN cells and primary microglial cells was used. $IFN-{\gamma}$ (0.1 -1 U/ml) stimulated phagocytosis in PMN cells 1.2 times after 2 - 3 h incubation, although at higher concentrations (10 - 100 U/ml) it strongly inhibited phagocytosis. In a similar way, at higher concentrations, $IFN-{\gamma}$ (100 - 500 U/ml) suppressed phagocytosis in zymosan-A stimulated microglial cells. When Polypodium leucotomus, cambricum and vulgare extracts were tested alone, increased levels of phagocytosis were observed in PMN. In addition, microglial cells showed both increased phagocytosis and MHC class-II antigen expressions. Surprisingly, when PMN and microglia were treated with a combination of Polypodium and $IFN-{\gamma}$, phagocytosis was not inhibited. We did not find changes in NO-synthase activity and nitrite production in both microglia and PMN cells activated by different immunomodulating agents. These results indicate that primary microglial cell cultures as well as human PMN cells can provide reproducible quantitative results in screening phagocytic activity of different immunoactive compounds. Furthermore, both inhibitory or activation mechanisms might be studied using these in vitro experimental approaches.

• Molecules and Cells
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• v.38 no.11
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• pp.998-1006
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• 2015

Retinols are metabolized into retinoic acids by alcohol dehydrogenase (ADH) and retinaldehyde dehydrogenase (Raldh). However, their roles have yet to be clarified in hepatitis despite enriched retinols in hepatic stellate cells (HSCs). Therefore, we investigated the effects of retinols on Concanavalin A (Con A)-mediated hepatitis. Con A was injected into wild type (WT), Raldh1 knockout ($Raldh1^{-/-}$), $CCL2^{-/-}$ and $CCR2^{-/-}$ mice. For migration study of regulatory T cells (Tregs), we used in vivo and ex vivo adoptive transfer systems. Blockade of retinol metabolism in mice given 4-methylpyrazole, an inhibitor of ADH, and ablated Raldh1 gene manifested increased migration of Tregs, eventually protected against Con A-mediated hepatitis by decreasing interferon-${\gamma}$ in T cells. Moreover, interferon-${\gamma}$ treatment increased the expression of ADH3 and Raldh1, but it suppressed that of CCL2 and IL-6 in HSCs. However, the expression of CCL2 and IL-6 was inversely increased upon the pharmacologic or genetic ablation of ADH3 and Raldh1 in HSCs. Indeed, IL-6 treatment increased CCR2 expression of Tregs. In migration assay, ablated CCR2 in Tregs showed reduced migration to HSCs. In adoptive transfer of Tregs in vivo and ex vivo, Raldh1-deficient mice showed more increased migration of Tregs than WT mice. Furthermore, inhibited retinol metabolism increased survival rate (75%) compared with that of the controls (25%) in Con A-induced hepatitis. These results suggest that blockade of retinol metabolism protects against acute liver injury by increased Treg migration, and it may represent a novel therapeutic strategy to control T cell-mediated acute hepatitis.