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Search Results: 1 - 10 of 41130 matches for " Ji-Won Lee "
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Investigation on the insecticidal limonoid content of commercial biopesticides and neem extract using solid phase extraction  [PDF]
Ji-Won Lee, Cho-Long Jin, Ki Chang Jang, Geun-Hyoung Choi, Hee-Dong Lee, Jin Hyo Kim
Journal of Agricultural Chemistry and Environment (JACEN) , 2013, DOI: 10.4236/jacen.2013.24012
Abstract: Neem extract is an alternative insecticide for organic farming and is an allowed component for commercial biopesticide in Korea. However, crop protection properties are not consistent in commercial products. In this report, quantitative analysis of commercial biopesticides for the four insecticidal limonoids of neem extract-azadirachtin A, azadirachtin B, deacetylsalannin and salannin, was conducted through solid phase extraction method with lipophilic-hydrophilic balanced material. The recoveries of the four limonoids ranged from 80.5% to 105%, and their limit of quantitation ranged from 0.028 mg/L to 0.356 mg/L. On the five imported neem extracts, the total contents of the four bioactive limonoids extracted were from 321 mg/L to 5810 mg/L, but there were big variations in the relative composition of the limonoids. The total limonoidal concentrations in 23 commercial bio-pesticides made from neem showed from below LOQ to 7190 mg/L with significant differences in the relative composition. These differences determine the biopesticide’s efficacy on pests, therefore, tracking the active ingredients is necessary for the quality control of commercial bio-pesticides.
Serum Carcinoembryonic Antigen Is Associated with Abdominal Visceral Fat Accumulation in Female Korean Nonsmokers
Jee-Yon Lee, Hyang-Kyu Lee, Duk-Chul Lee, Ji-Won Lee
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043518
Abstract: Background Carcinoembryonic antigen (CEA) is a tumor marker overexpressed in adenocarcinoma that has proinflammatory properties. Recent studies have reported that CEA is positively associated with carotid atherosclerosis and metabolic syndrome. Because visceral obesity is a known risk factor for cardiometabolic diseases, CEA may also be associated with visceral adiposity. Therefore, we investigated the relationship between serum CEA concentration and visceral obesity in female Korean nonsmokers. Methods A total of 270 Korean female nonsmokers were enrolled during their routine health check-ups. Biomarkers of metabolic risk factors were assessed along with body composition by computed tomography. Serum CEA levels were measured by using a chemiluminescence immunoassay analyzer. Results Serum CEA levels correlated with visceral fat area, fasting glucose, and triglyceride levels after adjusting for age and BMI. The mean visceral fat area increased significantly with the increasing CEA tirtiles. In a step-wise multiple regression analysis, age (β = 0.26, p<0.01) and visceral fat area (β = 0.19, p = 0.03) were identified as explanatory variables for serum CEA level. Conclusions This study suggested that CEA may be a mediator that links metabolic disturbance and tumorigenesis in visceral obesity. Further studies are required to better understand the clinical and pathophysiological significance of our findings.
Protective effect of the methanol extract from Cryptotaenia japonica Hassk. against lipopolysaccharide-induced inflammation in vitro and in vivo
Kang Hee,Bang Tae-Sun,Lee Ji-Won,Lew Jae-Hwan
BMC Complementary and Alternative Medicine , 2012, DOI: 10.1186/1472-6882-12-199
Abstract: Background In folk medicine, the aerial part of Crytotaenia japonica Hassk. (CJ), is applied for treatment of the common cold, cough, urinary problems, pneumonia, and skin rashes. In this paper, the in vitro and in vivo anti-inflammatory activity of CJ methanol extract was tested using lipopolysaccharide (LPS)-induced inflammatory models. Methods We measured nitric oxide (NO), inducible NO synthase (iNOS), and inflammatory cytokine levels from LPS-stimulated mouse peritoneal macrophages. Also, several cellular signaling molecules which regulate the expressions of these inflammatory markers were examined. Finally, we tested whether oral administration of CJ methanol extract might affect the serum cytokine levels in LPS-injected mice. Results CJ methanol extract reduced NO release via iNOS protein inhibition. The extract was also shown to decrease the secretions of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-12. Analysis of signaling molecules showed that CJ inhibited the phosphorylation of STAT1, p38, JNK and ERK1/2 as well as IκBα degradation. Finally, CJ decreased the serum levels of TNF-α and IL-6 in LPS-injected mice. Conclusions Our results demonstrated the anti-inflammatory activity of CJ methanol extract and its possible underlying mechanisms that involve modulation of IκBα, MAPK, and STAT1 activities.
DNA Methyltransferase Controls Stem Cell Aging by Regulating BMI1 and EZH2 through MicroRNAs
Ah-Young So,Ji-Won Jung,Seunghee Lee,Hyung-Sik Kim,Kyung-Sun Kang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0019503
Abstract: Epigenetic regulation of gene expression is well known mechanism that regulates cellular senescence of cancer cells. Here we show that inhibition of DNA methyltransferases (DNMTs) with 5-azacytidine (5-AzaC) or with specific small interfering RNA (siRNA) against DNMT1 and 3b induced the cellular senescence of human umbilical cord blood-derived multipotent stem cells (hUCB-MSCs) and increased p16INK4A and p21CIP1/WAF1 expression. DNMT inhibition changed histone marks into the active forms and decreased the methylation of CpG islands in the p16INK4A and p21CIP1/WAF1 promoter regions. Enrichment of EZH2, the key factor that methylates histone H3 lysine 9 and 27 residues, was decreased on the p16INK4A and p21CIP1/WAF1 promoter regions. We found that DNMT inhibition decreased expression levels of Polycomb-group (PcG) proteins and increased expression of microRNAs (miRNAs), which target PcG proteins. Decreased CpG island methylation and increased levels of active histone marks at genomic regions encoding miRNAs were observed after 5-AzaC treatment. Taken together, DNMTs have a critical role in regulating the cellular senescence of hUCB-MSCs through controlling not only the DNA methylation status but also active/inactive histone marks at genomic regions of PcG-targeting miRNAs and p16INK4A and p21CIP1/WAF1 promoter regions.
Combined Impact of Cardiorespiratory Fitness and Visceral Adiposity on Metabolic Syndrome in Overweight and Obese Adults in Korea
Sue Kim, Ji-Young Kim, Duk-Chul Lee, Hye-Sun Lee, Ji-Won Lee, Justin Y. Jeon
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0085742
Abstract: Background Obesity, especially visceral obesity, is known to be an important correlate for cardiovascular disease and increased mortality. On the other hand, high cardiorespiratory fitness is suggested to be an effective contributor for reducing this risk. This study was conducted to determine the combined impact of cardiorespiratory fitness and visceral adiposity, otherwise known as fitness and fatness, on metabolic syndrome in overweight and obese adults. Methods A total of 232 overweight and obese individuals were grouped into four subtypes according to their fitness level. This was measured by recovery heart rate from a step test in addition to visceral adiposity defined as the visceral adipose tissue area to subcutaneous adipose tissue area ratio (VAT/SAT ratio). Associations of fitness and visceral fatness were analyzed in comparison with the prevalence of metabolic syndrome. Results The high visceral fat and low fitness group had the highest prevalence of metabolic syndrome [Odds Ratio (OR) 5.02; 95% Confidence Interval (CI) 1.85–13.61] compared with the reference group, which was the low visceral adiposity and high fitness group, after adjustments for confounding factors. Viscerally lean but unfit subjects were associated with a higher prevalence of metabolic syndrome than more viscerally obese but fit subjects (OR 3.42; 95% CI 1.27–9.19, and OR 2.70; 95% CI 1.01–7.25, respectively). Conclusions Our study shows that visceral obesity and fitness levels are cumulatively associated with a higher prevalence of metabolic syndrome in healthy overweight and obese adults. This suggests that cardiorespiratory fitness is a significant modifier in the relation of visceral adiposity to adverse metabolic outcomes in overweight and obese individuals.
Dendropanoxide Induces Autophagy through ERK1/2 Activation in MG-63 Human Osteosarcoma Cells and Autophagy Inhibition Enhances Dendropanoxide-Induced Apoptosis
Ji-Won Lee, Kyoung-Sook Kim, Hyun-Kyu An, Cheorl-Ho Kim, Hyung-In Moon, Young-Choon Lee
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0083611
Abstract: Anticancer effects of dendropanoxide (DP) newly isolated from leaves and stem of Dendropanax morbifera Leveille were firstly investigated in this study. DP inhibited cell proliferation and induced apoptosis in dose- and time-dependent manner in MG-63 human osteosarcoma cells, which was dependent on the release of cytochrome c to the cytosol and the activation of caspases. Moreover, the DP-treated cells exhibited autophagy, as characterized by the punctuate patterns of microtubule-associated protein 1 light chain 3 (LC3) by confocal microscopy and the appearance of autophagic vacuoles by MDC staining. The expression levels of ATG7, Beclin-1 and LC3-II were also increased by DP treatment. Inhibition of autophagy by 3-methyladenine (3-MA) and wortmannin (Wort) significantly enhanced DP-induced apoptosis. DP treatment also caused a time-dependent increase in protein levels of extracellular signal-regulated kinase 1 and 2 (ERK1/2), and inhibition of ERK1/2 phosphorylation with U0126 resulted in a decreased DP-induced autophagy that was accompanied by an increased apoptosis and a decreased cell viability. These results indicate a cytoprotective function of autophagy against DP-induced apoptosis and suggest that the combination of DP treatment with autophagy inhibition may be a promising strategy for human osteosarcoma control. Taken together, this study demonstrated for the first time that DP could induce autophagy through ERK1/2 activation in human osteosarcoma cells and autophagy inhibition enhanced DP-induced apoptosis.
Metformin Represses Self-Renewal of the Human Breast Carcinoma Stem Cells via Inhibition of Estrogen Receptor-Mediated OCT4 Expression
Ji-Won Jung, Sang-Bum Park, Soo-Jin Lee, Min-Soo Seo, James E. Trosko, Kyung-Sun Kang
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0028068
Abstract: Metformin, a Type II diabetic treatment drug, which inhibits transcription of gluconeogenesis genes, has recently been shown to lower the risk of some diabetes-related tumors, including breast cancer. Recently, “cancer stem cells” have been demonstrated to sustain the growth of tumors and are resistant to therapy. To test the hypothesis that metformin might be reducing the risk to breast cancers, the human breast carcinoma cell line, MCF-7, grown in 3-dimensional mammospheres which represent human breast cancer stem cell population, were treated with various known and suspected breast cancer chemicals with and without non-cytotoxic concentrations of metformin. Using OCT4 expression as a marker for the cancer stem cells, the number and size were measured in these cells. Results demonstrated that TCDD (100 nM) and bisphenol A (10 μM) increased the number and size of the mammospheres, as did estrogen (10 nM E2). By monitoring a cancer stem cell marker, OCT4, the stimulation by these chemicals was correlated with the increased expression of OCT4. On the other hand, metformin at 1 and 10 mM concentration dramatically reduced the size and number of mammospheres. Results also demonstrated the metformin reduced the expression of OCT4 in E2 & TCDD mammospheres but not in the bisphenol A mammospheres, suggesting different mechanisms of action of the bisphenol A on human breast carcinoma cells. In addition, these results support the use of 3-dimensional human breast cancer stem cells as a means to screen for potential human breast tumor promoters and breast chemopreventive and chemotherapeutic agents.
Ginsenoside Rc Promotes Anti-Adipogenic Activity on 3T3-L1 Adipocytes by Down-Regulating C/EBPα and PPARγ
Ji-Won Yang,Sung Soo Kim
Molecules , 2015, DOI: 10.3390/molecules20011293
Abstract: Panax ginseng and its major components, the ginsenosides, are widely used in oriental medicine for the prevention of various disorders. In the present study, the inhibitory activity of ginsenoside Rc on adipogenesis was investigated using the 3T3-L1 cell line. The results obtained showed that Rc reduced the proliferation and viability of 3T3-L1 preadipocytes in a dose-dependent manner. Treatment with Rc decreased the number of adipocytes and reduced lipid accumulation in maturing 3T3-L1 preadipocytes, demonstrating an inhibitory effect on lipogenesis. Moreover, it was found that Rc directly induced lipolysis in adipocytes and down-regulated the expression of major transcription factors of the adipogenesis pathway, such as PPARγ and C/EBPα. These findings indicate that Rc is capable of suppressing adipogenesis and therefore they seem to be natural bioactive factors effective in adipose tissue mass modulation.
Impact of Diabetes on Oncologic Outcome of Colorectal Cancer Patients: Colon vs. Rectal Cancer
Justin Y. Jeon, Duck Hyoun Jeong, Min Geun Park, Ji-Won Lee, Sang Hui Chu, Ji-Hye Park, Mi Kyung Lee, Kaori Sato, Jennifer A. Ligibel, Jeffrey A. Meyerhardt, Nam Kyu Kim
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0055196
Abstract: Background To evaluate the impact of diabetes on outcomes in colorectal cancer patients and to examine whether this association varies by the location of tumor (colon vs. rectum). Patients and methods This study includes 4,131 stage I-III colorectal cancer patients, treated between 1995 and 2007 (12.5% diabetic, 53% colon, 47% rectal) in South Korea. Cox proportional hazards modeling was used to determine the prognostic influence of DM on survival endpoints. Results Colorectal cancer patients with DM had significantly worse disease-free survival (DFS) [hazard ratio (HR) 1.17, 95% confidence interval (CI): 1.00–1.37] compared with patients without DM. When considering colon and rectal cancer independently, DM was significantly associated with worse overall survival (OS) (HR: 1.46, 95% CI: 1.11–1.92), DFS (HR: 1.45, 95% CI: 1.15–1.84) and recurrence-free survival (RFS) (HR: 1.32, 95% CI: 0.98–1.76) in colon cancer patients. No association for OS, DFS or RFS was observed in rectal cancer patients. There was significant interaction of location of tumor (colon vs. rectal cancer) with DM on OS (P = 0.009) and DFS (P = 0.007). Conclusions This study suggests that DM negatively impacts survival outcomes of patients with colon cancer but not rectal cancer.
Chronic Resveratrol Treatment Protects Pancreatic Islets against Oxidative Stress in db/db Mice
Young-Eun Lee, Ji-Won Kim, Eun-Mi Lee, Yu-Bae Ahn, Ki-Ho Song, Kun-Ho Yoon, Hyung-Wook Kim, Cheol-Whee Park, Guolian Li, Zhenqi Liu, Seung-Hyun Ko
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0050412
Abstract: Resveratrol (RSV) has anti-inflammatory and anti-oxidant actions which may contribute to its cardiovascular protective effects. We examined whether RSV has any beneficial effects on pancreatic islets in db/db mice, an animal model of type 2 diabetes. The db/db and db/dm mice (non-diabetic control) were treated with (db-RSV) or without RSV (db-control) (20 mg/kg daily) for 12 weeks. After performing an intraperitoneal glucose tolerance test and insulin tolerance test, mice were sacrificed, the pancreas was weighed, pancreatic β-cell mass was quantified by point count method, and the amount of islet fibrosis was determined. 8-Hydroxydeoxyguanosine (8-OHdG), an oxidative stress marker, was determined in 24 h urine and pancreatic islets. RSV treatment significantly improved glucose tolerance at 2 hrs in db/db mice (P = 0.036), but not in db/dm mice (P = 0.623). This was associated with a significant increase in both pancreas weight (P = 0.011) and β-cell mass (P = 0.016). Islet fibrosis was much less in RSV-treated mice (P = 0.048). RSV treatment also decreased urinary 8-OHdG levels (P = 0.03) and the percentage of islet nuclei that were positive for 8-OHdG immunostaining (P = 0.019). We conclude that RSV treatment improves glucose tolerance, attenuates β-cell loss, and reduces oxidative stress in type 2 diabetes. These findings suggest that RSV may have a therapeutic implication in the prevention and management of diabetes.
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