• International Journal of Concrete Structures and Materials
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• v.18 no.3E
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• pp.145-150
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• 2006

An experiment with the objective of providing guidelines for joint depth determination and timing of contraction joint sawcutting to avert uncontrolled cement concrete pavement cracking has been conducted. Theoretical analysis and laboratory tests were performed to help in understanding and analyzing the field observation. Using two-dimensional elastic fracture mechanics, the influence of several parameters on crack propagation was delineated by a parametric study, involving initial notch ratio, joint spacing, Young's modulus and thermal expansion coefficient of concrete, temperature gradient, and modulus of subgrade reaction. Bimaterials made of rock plus cement mortar and rock plus polymer mortar were applied to the concrete in a field test section, and they were subjected to fracture tests. These tests have shown that fracture mechanics is a powerful tool not only in judging the quality of the jointed cement concrete pavement but also in providing a criterion for crack propagation and delamination. Based on fracture mechanics, a method is proposed to determine the joint depth, sawcut timing, and spacing of the jointed cement concrete pavement. This method has successfully been applied to a test section in Seohaean expressway. This study also summarizes the research results obtained from a field test for jointed plain concrete pavement, which was also carried out on the Seohaean expressway.

• Journal of Cancer Prevention
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• v.21 no.3
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• pp.135-143
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• 2016

Background: Fraxetin (7,8-dihydroxy-6-methoxy coumarin), a coumarin derivative, has been reported to possess antioxidative, anti-inflammatory and neuroprotective effects. A number of recent observations suggest that the induction of heme oxygenase-1 (HO-1) inhibits inflammation and tumorigenesis. In the present study, we determined the effect of fraxetin on HO-1 expression in HaCaT human keratinocytes and investigated its underlying molecular mechanisms. Methods: Reverse transcriptase-PCR and Western blot analysis were performed to detect HO-1 mRNA and protein expression, respectively. Cell viability was measured by the MTS test. The induction of intracellular reactive oxygen species (ROS) by fraxetin was evaluated by 2′,7′-dichlorofluorescin diacetate staining. Results: Fraxetin upregulated mRNA and protein expression of HO-1. Incubation with fraxetin induced the localization of nuclear factor-erythroid-2-related factor-2 (Nrf2) in the nucleus and increased the antioxidant response element-reporter gene activity. Fraxetin also induced the phosphorylation of Akt and AMP-activated protein kinase $(AMPK){\alpha}$ and diminished the expression of phosphatase and tensin homolog, a negative regulator of Akt. Pharmacological inhibition of Akt and $AMPK{\alpha}$ abrogated fraxetin-induced expression of HO-1 and nuclear localization of Nrf2. Furthermore, fraxetin generated ROS in a concentration-dependent manner. Conclusions: Fraxetin induces HO-1 expression through activation of Akt/Nrf2 or $AMPK{\alpha}/Nrf2$ pathway in HaCaT cells.

• Journal of Cancer Prevention
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• v.22 no.1
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• pp.1-5
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• 2017

Pancreatic cancer is a highly aggressive malignant tumor of the digestive system and radical resection, which is available to very few patients, might be the only possibility for cure. Since therapeutic choices are limited at the advanced stage, prevention is more important for reducing incidence in high-risk individuals with family history of pancreatic cancer. Epidemiological studies have shown that a high consumption of fish oil or ${\omega}3-polyunsaturated$ fatty acids reduces the risk of pancreatic cancers. Dietary fish oil supplementation has shown to suppress pancreatic cancer development in animal models. Previous experimental studies revealed that several hallmarks of cancer involved in the pathogenesis of pancreatic cancer, such as the resistance to apoptosis, hyper-proliferation with abnormal $Wnt/{\beta}-catenin$ signaling, expression of pro-angiogenic growth factors, and invasion. Docosahexaenoic acid (DHA) is a ${\omega}3-polyunsaturated$ fatty acid and rich in cold oceanic fish oil. DHA shows anti-cancer activity by inducing oxidative stress and apoptosis, inhibiting $Wnt/{\beta}-catenin$ signaling, and decreasing extracellular matrix degradation and expression of pro-angiogenic factors in pancreatic cancer cells. This review will summarize anti-cancer mechanism of DHA in pancreatic carcinogenesis based on the recent studies.

• Journal of Korean Academy of Nursing
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• v.27 no.4
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• pp.923-932
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• 1997

This study was done to analyze research trends and to suggest future perspectives for nursing research on meditation. The author reviewed 41 foreign research papers which had been published in the Journal of Consulting & Clinical Psychology(JCC) between 1966 and 1986, The Journal of Transpersonal Psychology(JTP) between 1967 and 1987, and The Journal of Counseling Psychology (JCP) between 1965 and 1994. The analysis of the studies focused on the concept of meditation, the type of study design, type of research subjects, type of meditation, the results of study, and the applied type of counseling and psychotherapy. The results of the study are summarized as follows : (1) When the study designs were analyzed six categories were identified (Literature reviews, Experiments, Surveys, Comparative study, Qualitative study, Others), and the majority of the studies were found to be Literature reviews (36.6%), or Experimental studies(39%), The number of studies on meditation has increased since the 1970's. (2) Most studies approached meditation with Zen and Yoga(72.5%) which were called concepts of Indian meditation from 1970's to the later of 1980's. TM(Transcendental Meditation) was used in the 1970's. (3) On the type of meditation, most studies used Zen meditation which was called a method of Buddhistic meditation(43.9%). (4) On the studies of meditation effect, most were about psychological changes(48.5%), and psychological changes and physiological changes(37.1%). (5) On the types of the study subjects it was found that 15 studies dealt with literature, nine studies investigated college students, and eight studies investigated the meditator. (6) Most of study showed the results of the meditation effect to be positive (80%). On the basis of the above findings the following recommendations are made : (1) It's necessary to do a reliable and variable analysis of research trends on meditation. (2) There is a need to study the effects of meditation in order to clarify meditation application in counseling.

• Journal of Cancer Prevention
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• v.22 no.4
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• pp.234-240
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• 2017

Background: Lung cancer is the leading cause of cancer-related death worldwide, for which smoking is considered as the primary risk factor. The present study was conducted to determine whether genetic alterations induced by radon exposure are associated with the susceptible risk of lung cancer in never smokers. Methods: To accurately identify mutations within individual tumors, next generation sequencing was conduct for 19 pairs of lung cancer tissue. The associations of germline and somatic variations with radon exposure were visualized using OncoPrint and heatmap graphs. Bioinformatic analysis was performed using various tools. Results: Alterations in several genes were implicated in lung cancer resulting from exposure to radon indoors, namely those in epidermal growth factor receptor (EGFR), tumor protein p53 (TP53), NK2 homeobox 1 (NKX2.1), phosphatase and tensin homolog (PTEN), chromodomain helicase DNA binding protein 7 (CHD7), discoidin domain receptor tyrosine kinase 2 (DDR2), lysine methyltransferase 2C (MLL3), chromodomain helicase DNA binding protein 5 (CHD5), FAT atypical cadherin 1 (FAT1), and dual specificity phosphatase 27 (putative) (DUSP27). Conclusions: While these genes might regulate the carcinogenic pathways of radioactivity, further analysis is needed to determine whether the genes are indeed completely responsible for causing lung cancer in never smokers exposed to residential radon.

• Journal of Cancer Prevention
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• v.21 no.2
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• pp.88-94
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• 2016

Background: Breast cancer is the most common malignant disease in women. The patients with advanced breast cancer develop metastasis to bone. Bone metastasis and skeletal-related events by breast cancer are frequently associated with the invasiveness of breast cancer cells and osteoclasts-mediated bone resorption. Forsythia koreana is used in oriental traditional medicine to treat asthma, atopy, and allergic diseases. The aim of this study was to evaluate the inhibitory effects of F. koreana extracts on the invasion of breast cancer cells and bone resorption by osteoclasts. Methods: Cell viability was measured by an MTT assay and the migration and invasion of MDA-MB-231 cells were detected by a Boyden chamber assay. The formation of osteoclasts and pit was detected using tartrate-resistant acid phosphatase staining and calcium phosphate-coated plates, respectively. The activities of matrix metalloproteinases (MMPs) and cathepsin K were evaluated by gelatin zymography and a cathepsin K detection kit. Results: The fruit and leaf extracts of F. koreana significantly inhibited the invasion of MDA-MB-231 cells at noncytotoxic concentrations. The fruit extract of F. koreana reduced the transforming growth factor ${\beta}1-induced$ migration, invasion and MMPs activities of MDA-MB-231 cells. In addition, the fruit, branch, and leaf extracts of F. koreana also inhibited the receptor activator of nuclear factor kappa-B ligand-induced osteoclast formation and osteoclast-mediated bone-resorbing activity by reducing the activities of MMPs and cathepsin K. Conclusions: The extracts of F. koreana may possess the potential to inhibit the breast cancer-induced bone destruction through blocking invasion of breast cancer cells, osteoclastogenesis, and the activity of mature osteoclasts.

• Journal of Cancer Prevention
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• v.21 no.2
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• pp.95-103
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• 2016

Background: Excess energy supply induces chronic low-grade inflammation in association with oxidative stress in various tissues including intestinal epithelium. The objective of this study was to investigate the effect of high-fat diet (HFD) on intestinal cell membrane integrity and intestinal tumorigenesis in $Apc^{Min/+}$ mice. Methods: Mice were fed with either normal diet (ND) or HFD for 12 weeks. The number of intestinal tumors were counted and biomarkers of endotoxemia, oxidative stress, and inflammation were determined. Changes in intestinal integrity was measured by fluorescein isothiocyanate (FITC)-dextran penetration and membrane gap junction protein expression. Results: HFD group had significantly higher number of tumors compared to ND group (P < 0.05). Blood total antioxidant capacity was lower in HFD group, while colonic 8-hydroxy-2'-deoxyguanosine level, a marker of oxidative damage, was higher in HFD group compared to that of ND group (P < 0.05). The penetration of FITC-dextran was substantially increased in HFD group (P < 0.05) while the expressions of membrane gap junction proteins including zonula occludens-1, claudin-1, and occludin were lower in HFD group (P < 0.05) compared to those in ND group. Serum concentration of lipopolysaccharide (LPS) receptor (CD14) and colonic toll-like receptor 4 (a LPS receptor) mRNA expression were significantly higher in HFD group than in ND group (P < 0.05), suggesting that significant endotoxemia may occur in HFD group due to the increased membrane permeability. Serum interleukin-6 concentration and myeloperoxidase activity were also higher in HFD group compared to those of ND group (P < 0.05). Conclusions: HFD increases oxidative stress disrupting intestinal gap junction proteins, thereby accelerating membrane permeability endotoxemia, inflammation, and intestinal tumorigenesis.

• Journal of Cancer Prevention
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• v.21 no.3
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• pp.144-151
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• 2016

Background: Immunoregulatory elements have emerged as useful immunotherapeutic agents against cancer. In traditional medicine, Mori folium, the leaf of Morus alba L. (Moraceae), has been used for various medicinal purposes; however, the immunomodulatory effects have not been fully identified. We evaluated the immunoenhancing potential of water extract of Mori folium (WEMF) in murine RAW264.7 macrophages. Methods: RAW264.7 cells were treated with WEMF for 24 hours and cell viability was detected by an MTT method. Nitric oxide (NO) levels in the culture supernatants were assayed using Griess reagent. The productions of prostaglandin $E_2$ ($PGE_2$) and immune-related cytokines was measured using ELISA detection kits. The mRNA and protein expression levels of Inducible NO synthase, COX-2, and cytokines were assayed by reverse transcription-PCR and Western blotting, respectively. The effect of WEMF on phagocytic activity was measured using a Phagocytosis Assay Kit. Results: WEMF significantly stimulated the production of NO and $PGE_2$ as immune response parameters at noncytotoxic concentrations, which was associated with the increased expression of inducible NO synthase and COX-2. The release and expression of cytokines, such as $TNF-{\alpha}$, interleukin $(IL)-1{\beta}$, IL-6, and IL-10, were also significantly increased in response to treatment with WEMF. Moreover, WEMF promoted the macrophagic differentiation of RAW264.7 cells and the resulting phagocytosis activity. Conclusions: WEMF has the potential to modulate the immune function by regulating immunological parameters. Further studies are needed to identify the active compounds and to support the use of WEMF as an immune stimulant.

• Journal of Cancer Prevention
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• v.23 no.4
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• pp.191-196
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• 2018

Background: Type 2 diabetes mellitus (T2DM) and cancer are serious health problems worldwide, and their prevalences have been on the rise in recent years. It has been reported that adropin plays an important role in the development of T2DM, oxidative stress, inflammation, and obesity. However, there is limited information available on T2DM from human studies, especially for the Korean population. In this study, we aimed to investigate the correlation between adropin levels and obesity of Korean T2DM patients. Methods: Thirty-six T2DM patients were recruited for this study. The participants were further classified into female (n = 12) and male (n = 24). Their body composition, metabolic parameters, inflammatory factors, and oxidative stress were measured. Results: The severity of obesity is more manifested in male than in female. Plasma triglyceride (TG) and high-sensitivity C-reactive protein (hs-CRP) levels of male were significantly higher than female. The plasma adropin and adiponectin level of female was significantly higher than male. The body weight, body mass index (BMI), body fat mass were negatively correlated with the plasma adropin level in female, whereas adropin has positive correlation with adiponectin in female. The hs-CRP was negatively correlated with the plasma adropin level in female and male. malondialdehyde, reactive oxidative species, and $TNF-{\alpha}$ was not significantly correlated with adropin in patients with T2DM. Conclusions: These findings suggest that adropin may be more used as a biomarker for predicting the risk of obesity and inflammation in Korean patients with T2DM, especially women.

• Journal of Cancer Prevention
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• v.23 no.4
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• pp.170-175
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• 2018

Background: Human hepatocellular carcinoma (HCC) is a common liver tumor and the main cause of cancer-related death. Tyrosine kinase inhibitors, such as imatinib and GNF5 which were developed to treat chronic myelogenous leukemia, regulate the progression of various cancers. The aim of this study was to confirm the anti-tumor activity of tyrosine kinase inhibitors through regulation of S-phase kinase-associated protein 2 (Skp2), an important oncogenic factor in various cancer cells, in human hepatocarcinoma SK-HEP1 cells. Methods: Cell viability and colony formation assays were conducted to evaluate the effects of imatinib, GNF5 and GNF2 on the growth of SK-HEP1 cells. Using immunoblot analysis, we assessed change of the activation of caspases, PARP, Akt, mitogen-activated protein kinases, and Skp2/p27/p21 pathway by imatinib and GNF5 in SK-HEP1 cells. Using sh-Skp2 HCC cells, the role of Skp2 in the effects of imatinib and GNF5 was evaluated. Results: Imatinib and GNF5 significantly inhibited the growth of SK-HEP1 cells. Treatment of imatinib and GNF5 decreased Skp2 expression and Akt phosphorylation, and increased the expression of p27, p21, and active-caspases in SK-HEP1 cells. In sh-Skp2 HCC cells, cell growth and the expression of Skp2 were inhibited by more than in the mock group treated with imatinib and GNF5. Conclusions: These results suggest that the anti-growth activity of tyrosine kinase inhibitors may be associated with the regulation of p27/p21 and caspases through Skp2 blockage in HCC cells.