• Korean Journal of Weed Science
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• v.30 no.1
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• pp.43-49
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• 2010

This study was conducted to predict the rice yield loss and determine the economic threshold levels for water direct seeded rice from competition of the most serious weeds, Scirpus juncoides Roxb. (bulrush) and Echinochlor crusgalli L. (barnyardgrass) in Daegu of Korea. To predict crop yield as a function of weed density used a rectangular hyperbola, and determine their economic threshold levels used the equation developed by Cousens. The rice yield loss model of S. juncoides was predicted as y = 466 / (1+0.00188x), $R^2$ = 0.933 and that of E. crusgalli was y = 458 / (1+0.02402x), $R^2$ = 0.973. In comparison of the competitiveness represented by parameter ${\beta}$, it was 0.001884 in S. juncoides and 0.02402 in E. crusgalli. Economic threshold calculated using Cousens' equation was negatively related to the competitiveness of weed. So that the economic threshold of S. juncoides was 13.4 and that of E. crusgalli was 1.07 plants per $m^2$.

• Journal of Environmental Health Sciences
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• v.37 no.6
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• pp.450-459
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• 2011

Objectives: Biomarkers in urine are important in assessing exposures to environmental or occupational chemicals and for evaluateing renal function by exposure from these chemicals. Spot urine samples are needed to adjust the concentration of these biomarkers for variations in urine dilution. This study was conducted to evaluate the suitability of adjusting the urinary concentration of cadmium (uCd) and arsenic (uAs) by specific gravity (SG) and urine creatinine (uCr). Methods: We measured the concentrations of blood cadmium (bCd), uCd, uAs, uCr, SG and N-acetyl-${\beta}$-D-glucosaminidase (NAG) activity, which is a sensitive marker of tubular damage by low dose Cd exposure, in spot urine samples collected from 536 individuals. The value of uCd, uAs and NAG were adjusted by SG and uCr. Results: The uCr levels were affected by gender (p < 0.01) and muscle mass (p < 0.01), while SG levels were affected by gender (p < 0.05). Unadjusted uCd and uAs were correlated with SG (uCd: r = 0.365, p < 0.01; uAs: r = 0.488, p < 0.01), uCr (uCd: r = 0.399, p < 0.01; uAs: r = 0.484, p < 0.01). uCd and uAs adjusted by SG were still correlated with SG (uCd: r = 0.360, p < 0.01, uAs: r = 0.483, p < 0.01). uCd and uAs adjusted by uCr and modified uCr ($M_{Cr}$) led to a significant negative correlation with uCr (uCd: r = -0.367, p < 0.01; uAs: r = -0.319, p < 0.01) and $M_{Cr}$ (uCd: r = -0.292, p < 0.01; uAs: r = -0.206, p < 0.01). However, uCd and uAs adjusted by conventional SG ($C_{SG}$) were disappeared from these urinary dilution effects (uCd: r = -0.081; uAs: r = 0.077). Conclusions: $C_{SG}$ adjustment appears to be more appropriate for variations in cadmium and arsenic in spot urine.

• Asian-Australasian Journal of Animal Sciences
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• v.13 no.10
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• pp.1359-1366
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• 2000

An experiment was carried out to study plasma levels of hormones and metabolites of crossbred Holstein cattle during late pregnancy (28 days pre partum), early lactation (30 days post partum), mid-lactation (120 days post partum) and late lactation (210 days post partum). Two breed types of Holstein $Friesian{\times}Red$ Sindhi (50:50 = 50%HF) and Holstein $Friesian{\times}Red$ Sindhi (87.5:12.5 = 87.5%HF) were divided into four groups of four animals each. Two groups of each breed were fed with either rice straw treated with 5% urea or pangola hay (Digitaria decumbens) as the source of roughage throughout the experiments. There were a substantial increases in the mean levels of total triiodothyronine ($T_3$), insulin and glucagon at the onset of lactation, and maintained in a high levels during lactation advance for all groups of experiments. The mean levels of prolactin and thyroxine ($T_4$) were not significantly different among groups of animals, but the plasma cortisol concentration was slightly higher in both groups of 50%HF in comparison with those of 87.5%HF animals. The mean levels of plasma growth hormone (GH) of both groups of 87.5%HF animals feeding on either hay or urea treated rice straw markedly rose in the early period of lactation and markedly reduced in mid- and late lactation. These changes were accompanied with changes of milk yield. In contrast to 50%HF animals, plasma GH levels were considerably higher in the late pregnant period than in the early period of lactation and it remained constant as its value at the early lactation throughout the experimental period. The high levels of both plasma progesterone and estradiol concentration significantly declined after parturition and remained low through lactating period. The plasma glucose level in the 50%HF animals feeding on either hay or urea treated rice straw was higher than the 87.5%HF animals in all periods of experiments. Changes in plasma FFA levels of both types of crossbred animals were depended on the endocrine status during late pregnancy and lactation. The levels of plasma FFA of 50%HF animals were significantly higher (p<0.05) than those of 87.5%HF animals during late pregnancy. Both plasma ${\beta}$-hydroxybutyrate and lactate concentrations were not affected by feeding on either hay or urea treated rice straw during late pregnancy and lactation. These data demonstrate that there were no differences in the physiological performances in the same crossbred animals fed either hay or urea treated rice straw. The 87.5%HF animal has the genetic potential for a high milk yield and homeorhetic adaptation for mammary function differed from 50%HF animals during periods of lactation. Altering lactation persistency in 87.5%HF is regulated mainly by chronically acting growth hormones through the period of lactation.

• The Korean Journal of Physiology and Pharmacology
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• v.9 no.2
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• pp.103-108
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• 2005

To study the direct effect of somatostatin (SS) on calcium channel current ($I_{Ba}$) in guinea-pig gastric myocytes, $I_{Ba}$ was recorded by using whole-cell patch clamp technique in single smooth muscle cells. Nicardipine ($1{\mu}M$), a L-type $Ca^{2+}$ channel blocker, inhibited $I_{Ba}$ by $98{\pm}1.9$% (n=5), however $I_{Ba}$ was decreased in a reversible manner by application of SS. The peak $I_{Ba}$ at 0 mV were decreased to $95{\pm}1.5$, $92{\pm}1.9$, $82{\pm}4.0$, $66{\pm}5.8$, $10{\pm}2.9$% at $10^{-10}$, $10^{-9}$, $10^{-8}$, $10^{-7}$, $10^{-5}$ M of SS, respectively (n=3∼6; $mean{\pm}SEM$). The steady-state activation and inactivation curves of $I_{Ba}$ as a function of membrane potentials were well fitted by a Boltzmann equation. Voltage of half-activation ($V_{0.5}$) was $-12{\pm}0.5$ mV in control and $-11{\pm}1.9$ mV in SS treated groups (respectively, n=5). The same values of half-inactivation were $-35{\pm}1.4$ mV and $-35{\pm}1.9$ mV (respectively, n=5). There was no significant difference in activation and inactivation kinetics of $I_{Ba}$ by SS. Inhibitory effect of SS on $I_{Ba}$ was significantly reduced by either dialysis of intracellular solution with $GDP_{\beta}S$, a non-hydrolysable G protein inhibitor, or pretreatment with pertussis toxin (PTX). SS also decreased contraction of guinea-pig gastric antral smooth muscle. In conclusion, SS decreases voltage-dependent L-type calcium channel current ($VDCC_L$) via PTXsensitive signaling pathways in guinea-pig antral circular myocytes.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.661-670
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• 2018

Fimasartan, a new angiotensin II receptor antagonist, reduces myocyte damage and stabilizes atherosclerotic plaque through its anti-inflammatory effect in animal studies. We investigated the protective effects of pretreatment with fimasartan on ischemia-reperfusion injury (IRI) in a mouse model of ischemic renal damage. C57BL/6 mice were pretreated with or without 5 (IR-F5) or 10 (IR-F10) mg/kg/day fimasartan for 3 days. Renal ischemia was induced by clamping bilateral renal vascular pedicles for 30 min. Histology, pro-inflammatory cytokines, and apoptosis assays were evaluated 24 h after IRI. Compared to the untreated group, blood urea nitrogen and serum creatinine levels were significantly lower in the IR-F10 group. IR-F10 kidneys showed less tubular necrosis and interstitial fibrosis than untreated kidneys. The expression of F4/80, a macrophage infiltration marker, and tumor necrosis factor $(TNF)-{\alpha}$, decreased in the IR-F10 group. High-dose fimasartan treatment attenuated the upregulation of $TNF-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 in ischemic kidneys. Fewer TUNEL positive cells were observed in IR-F10 compared to control mice. Fimasartan caused a significant decrease in caspase-3 activity and the level of Bax, and increased the Bcl-2 level. Fimasartan preserved renal function and tubular architecture from IRI in a mouse ischemic renal injury model. Fimasartan also attenuated upregulation of inflammatory cytokines and decreased apoptosis of renal tubular cells. Our results suggest that fimasartan inhibited the process of tubular injury by preventing apoptosis induced by the inflammatory pathway.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.18 no.8
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• pp.285-293
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• 2017

The purpose of this study is to examine the relationship between the Minnesota Multiphasic Personality Inventory(MMPI-2) clinical scales and the self-regulation quotient of the brain quotient. The test in this study was performed by 41 adults over 20 years old and was done using the MMPI-2, which is a self-reporting method. EEG was performed using a 2-channel EEG System at Fp1 and Fp2. The analysis showed a negative correlation between scale 2(D), which is the MMPI-2 clinical scale, and the SRQ(Self Regulation Quotient) relaxation status, which is the related alpha rhythm. Scale3(Hy) showed a positive correlation with the SRQ concentration status and low ${\beta}$ rhythm. Scale7 in the MMPI-2 clinical scales showed a negative correlation with the SRQ relaxation status, which is the alpha rhythm. This means that MMPI-2 and SRQ can be used complementarily in the field of counseling. These results could be interpreted in three ways. First, people with depression are sensitive to other people's attention and evaluation. Therefore, they tend to expend a lot of energy when forming interpersonal relationships, and if they do not learn to relax, their fatigue can easily be increased. Second, people who seek other people's interest and have a cheerful spirit are considered to be highly active. Third, highly stressed people with anxiety and tension seem to easily become tired and their irritation and discomfort may be increased in consequence.

• The Korean Journal of Physiology and Pharmacology
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• v.18 no.3
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• pp.255-261
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• 2014

Essential fatty acid (EFA) is known to be required for the body to function normally and healthily. However, the effect of EFA on glucose uptake in skeletal muscle has not yet been fully investigated. In this study, we examined the effect of two EFAs, linoleic acid (LA) and ${\alpha}$-linolenic acid (ALA), on glucose uptake of C2C12 skeletal muscle cells and investigated the mechanism underlying the stimulatory effect of polyunsaturated EFAs in comparison with monounsaturated oleic acid (OA). In palmitic acid (PA)-induced insulin resistant cells, the co-treatment of EFAs and OA with PA almost restored the PA-induced decrease in the basal and insulin-stimulated 2-NBDG (fluorescent D-glucose analogue) uptake, respectively. Two EFAs and OA significantly protected PA-induced suppression of insulin signaling, respectively, which was confirmed by the increased levels of Akt phosphorylation and serine/threonine kinases ($PKC{\theta}$ and JNK) dephosphorylation in the western blot analysis. In PA-untreated, control cells, the treatment of $500{\mu}M$ EFA significantly stimulated 2-NBDG uptake, whereas OA did not. Phosphorylation of AMP-activated protein kinase (AMPK) and one of its downstream molecules, acetyl-CoA carboxylase (ACC) was markedly induced by EFA, but not OA. In addition, EFA-stimulated 2-NBDG uptake was significantly inhibited by the pre-treatment of a specific AMPK inhibitor, adenine 9-${\beta}$-D-arabinofuranoside (araA). These data suggest that the restoration of suppressed insulin signaling at PA-induced insulin resistant condition and AMPK activation are involved at least in the stimulatory effect of EFA on glucose uptake in C2C12 skeletal muscle cells.

• Nutrition Research and Practice
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• v.1 no.2
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• pp.105-112
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• 2007

Ascorbic acid has been reported to extend replicative life span of human embryonic fibroblast (HEF). Since the detailed molecular mechanism of this phenomenon has not been investigated, we attempted to elucidate. Continuous treatment of HEF cells with ascorbic acid at ($200{\mu}M$) from 40 population doubling (PD) increased maximum PD numbers by 18% and lowered $SA-{\beta}-gal$ positive staining, an aging marker, by 2.3 folds, indicating that ascorbic acid extends replicative life span of HEF cells. Ascorbic acid treatment lowered DCFH by about 7 folds and Rho123 by about 70%, suggesting that ascorbic acid dramatically decreased ROS formation. Ascorbic acid also increased aconitase activity, a marker of mitochondrial aging, by 41%, indicating that ascorbic acid treatment restores age-related decline of mitochondrial function. Cell cycle analysis by flow cytometry revealed that ascorbic acid treatment decreased G1 population up to 12%. Further western blot analysis showed that ascorbic acid treatment decreased levels of p53, phospho-p53 at ser 15, and p21, indicating that ascorbic acid relieved senescence-related G1 arrest. Analysis of AP (apurinic/apyrimidinic) sites showed that ascorbic acid treatment decreased AP site formation by 35%. We also tested the effect of hydrogen peroxide treatment, as an additional oxidative stress. Continuous treatment of $20{\mu}M$ of hydrogen peroxide from PD 40 of HEF cells resulted in premature senescence due to increased ROS level, and increased AP sites. Taken together, the results suggest that ascorbic acid extends replicative life span of HEF cells by reducing mitochondrial and DNA damages through lowering cellular ROS.

• The Korean Journal of Pesticide Science
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• v.9 no.2
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• pp.140-145
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• 2005

Quantitative Structure Activity Relationship (QSAR) assumes the relatedness between physical property and biological activity. However, activity data measured at single concentration such as percent activity have not been used extensively for modeling purpose. This probably comes from the fact that these values are qualitative instead of quantitative. To utilize percent activity data for molecular modeling, we classified the whole data into two classes. One class represents the active while the other signifies the inactive. The percent activity data of ${\beta}$-Ketoacetoanilides measured for TLB (Tomato Late Blight) were investigated. CoMFA (Comparative Molecular Field Analysis) was used as a discriminant function. Using CoMFA provides 3D (three dimensional) information, which is crucial for chemical insight. It can also serve as a predictive model. The resultant model classified the given data correctly (98%). When LOO (leave-one-out) crossvalidation procedure was applied, the classification accuracy was 69%. Therefore two class approximation of percent activity data with CoMFA can be utilized to understand the relationship between chemical structure and biological activity and design subsequent chemical analogs.

• IMMUNE NETWORK
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• v.3 no.3
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• pp.201-210
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• 2003

Objective: The role of prostaglandin $E_2$ (PGE2) in the etiopathogenesis of immune and inflammatory diseases has become the subject of recent debate. To determine the role of PGE2 in rheumatoid arthritis (RA), we tested the effect of exogenous PGE2 on the production of cyclooxygenase-2 (COX-2) by rheumatoid synoviocytes. Methods: Fibroblast-like synoviocytes (FLS) were prepared from the synovial tissues of RA patients, and cultured in the presence of PGE2. The COX-2 mRNA and protein expression levels were determined by RT-PCR and Western blot analysis, respectively. The PGE2 receptor subtypes in the FLS were analyzed by RT-PCR. Electrophoretic mobility shift assay (EMSA) was used to measure the NF-${\kappa}B$ binding activity for COX-2 transcription. The in vivoeffect of PGE2 on the development of arthritis was also tested in collagen induced arthritis (CIA) animals. Results: PGE2 ($10^{-11}$ to $10^{-5}M$) dose-dependently inhibited the expression of COX-2 mRNA and the COX-2 protein stimulated with IL-$1{\beta}$, but not COX-1 mRNA. NS-398, a selective COX-2 inhibitor, displayed an additive effect on PGE2-induced COX-2 downregulation. The FLS predominantly expressed the PGE2 receptor (EP) 2 and EP4, which mediated the COX-2 suppression by PGE2. Treatment with anti-IL-10 monoclonal antibodies partially reversed the PGE2-induced suppression of COX-2 mRNA, suggesting that IL-10 may be involved in modulating COX-2 by PGE2. Experiments using an inducer and an inhibitor of cyclic AMP (cAMP) suggest that cAMP is the major intracellular signal that mediates the regulatory effect of PGE2 on COX-2 expression. EMSA revealed that PGE2 inhibited the binding of NF-${\kappa}B$ in the COX-2 promoter via a cAMP dependent pathway. In addition, a subcutaneous injection of PGE2 twice daily for 2 weeks significantly reduced the incidence and severity of CIA as well as the production of IgG antibodies to type II collagen. Conclusion: Our data suggest that overproduced PGE2 in the RA joints may function as an autocrine regulator of its own synthesis by inhibiting COX-2 production and may, in part, play an anti-inflammatory role in the arthritic joints.