• Herbal Formula Science
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• v.26 no.3
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• pp.223-236
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• 2018

Objectives : We compared the inhibitory effects of herb-combined remedies, which were recorded on "Yooam" prescription of Dongeuibogam, on cell migration and invasion, two critical cellular processes that are often deregulated during metastasis, in B16F10 melanoma cells. For this purpose, water extracts of Sipyukmiryukieum (SYMRKU), Danjacheongpitang (DJCPT), Cheongganhaeultang (CGHUT) and Jipaesan (JPS) were used. Methods : Cytotoxicity was assessed by an MTT assay. Wound healing and matrigel transwell assays were used to examine on B16F10 cell migration and invasion. The levels of mRNA and protein expression of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) were analyzed by RT-PCR and Western blotting. Results : Our data showed that DJCPT showed the strongest inhibitory effect among the four prescriptions in inhibiting cell motility of B16F10 melanoma cells within the concentration range that was not cytotoxic. The inhibitory potential of colony formation was higher in DJCPT and SYMRKU compared to the other two types of prescriptions, and the inhibitory effect of invasiveness is shown in order of DJCPT, SYMRKU, CGHUT and JPS. DJCPT, and SYMRKU strongly inhibited the activity and expression of MMP-2 and MMP-9, which are important mediators in cancer invasion, compared to CGHUT and JPS, and the increased expression of TIMP-1 and TIMP-2 was also more effective in these two prescriptions. In conclusion, DJCPT is expected to exhibit the most potent blocking effect on migration and invasion among four herb-combined remedies compared in B16F10 melanoma cells. Conclusion : Overall, the results of this study will be used as an important source to validate these prescriptions in animal models and to understand the mechanism of action of herbal remedies recorded in Dongeuibogam.

• Journal of Preventive Medicine and Public Health
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• v.38 no.3
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• pp.283-290
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• 2005

Objectives : The aim of this paper was to examine the relationship between the summertime (June to August) heat index, which quantifies the bioclimatic apparent temperature in sultry weather, and the daily disease-related mortality in Seoul for the period from 1991 to 2000. Methods : The daily maximum (or minimum) summertime heat indices, which show synergetic apparent temperatures, were calculated from the six hourly temperatures and real time humidity data for Seoul from 1991 to 2000. The disease-related daily mortality was extracted with respect to types of disease, age and sex, etc. and compared with the time series of the daily heat indices. Results : The summertime mortality in 1994 exceeded the normal by 626 persons. Specifically, blood circulation-related and cancer-related mortalities increased in 1994 by 29.7% (224 persons) and 15.4% (107 persons), respectively, compared with those in 1993. Elderly persons, those above 65 years, were shown to be highly susceptible to strong heat waves, whereas the other age and sex-based groups showed no significant difference in mortality. In particular, a heat wave episode on the 22nd of July 2004 ($>45^{\circ}C$ daily heat index) resulted in double the normal number of mortalities after a lag time of 3 days. Specifically, blood circulation-related mortalities, such as cerebral infraction, were predominant causes. Overall, a critical mortality threshold was reached when the heat index exceeded approximately $37^{\circ}C$, which corresponds to human body temperature. A linear regression model based on the heat indices above $37^{\circ}C$, with a 3 day lag time, accounted for 63% of the abnormally increased mortality (${\geq}+2$ standard deviations). Conclusions : This study revealed that elderly persons, those over 65 years old, are more vulnerable to mortality due to abnormal heat waves in Seoul, Korea. When the daily maximum heat index exceeds approximately $37^{\circ}C$, blood circulation-related mortality significantly increases. A linear regression model, with respect to lag-time, showed that the heat index based on a human model is a more dependable indicator for the prediction of hot weather-related mortality than the ambient air temperature.

• Korean Journal of Head & Neck Oncology
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• v.22 no.2
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• pp.130-136
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• 2006

Introduction : The sensitivity of tumor cells to radiotherapy is a critical determinant of local control and potential cure in advanced head and neck squamous cell carcinoma(HNSCC). The emergence of radioresistant tumor cells is an obstacle to cancer therapy. Most radioresistant cells have a higher proportion of cells in the Sphase of the cell cycle and a lower apoptotic fraction than radiosensitive cells. HSV replication is increased in cells that have higher S-phase fractions. NV1066 is an oncolytic herpes simplex virus type-1 mutant. We hypothesized that NV1066 replication and cytotoxicity are increased in radioresistant cells. The purpose of this study is to evaluate the antitumor efficacy of NV1066 to treat radioresistant HNSCC. Methods : Radioresistant cells were selected by treating five HNSCC cell lines with repeated conventional fractionated doses of radiation(2Gy/day), using a Cs-137 irradiator, up to a cumulative dose of 70Gy. Clonogenic cell survival and S-phase fractions were compared between radioresistant and parental radiosensitive cells. The two cell populations were then treated with NV1066 to examine viral replication, by the viral plaque assay and viral cytotoxicity. Results : Fractionated irradiation resulted in the selection of radioresistant cells. Radioresistant cells had a higher S-phase fraction(42.9%) compared to parental cells(26.2%). NV1066 replication in radioresistant cells was 7.4 times higher than in parental cells(p<0.01). Treatment with NV1066 resulted in increased cytotoxicity of 24.5% in radioresistant cells compared to parental cells(p<0.05). Conclusion : NV1066 showed increased viral replication and cytotoxicity in radioresistant HNSCC cell lines. These findings suggest a potential clinical application for this oncolytic viral therapy as treatment for radioresistant head and neck cancers.

• The Journal of Internal Korean Medicine
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• v.39 no.4
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• pp.662-675
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• 2018

Objective: The aim of this study was to establish the developmental history of hospice palliative care (HPC) with Korean medicine (KM). Methods: We compared the developmental history of HPC in Korea with that of Britain, the United States, Taiwan, Japan, and China. The articles in English or Korean published until Feb. 2017 were searched using 'Hospice' or 'Palliative care' with the name of each nation in the PubMed, MEDLINE, ScienceDirect, and CINAHL (Cumulative Index to Nursing and Allied Health Literature) databases for foreign articles and OASIS (Oriental Medicine Advanced Searching Integrated System) for domestic articles. Books and gray literature were searched on the same databases and websites of the Ministry of Health and Welfare and related organizations in each country. Results: Modern palliative care began with the hospice movement led by Dr. Cicely Saunders. HPC in Korea started earlier than in other countries but it took considerable time for social consensus, so Korean policies have only been published recently. In this process, KM was excluded from HPC. For this reason, western medicine in Korea does not fully accept the spirit of HPC, the government does not take an aggressive stance with KM, and the institutes of KM do not have any interest in HPC. The World Health Organization recommends the establishment of policies and programs connected with a country's own health care system. In 2015, the Korean government made the third comprehensive plan for the development of KM. It included critical pathway guidelines about cancer-related fatigue and anorexia. More effort is required to set up HPC than other care types because Korea has two medical systems. Conclusions: Each nation has been trying to improve systems of HPC. We need to overcome the problems and bring out the best by making our own model of HPC with KM.

• The Journal of the Korean bone and joint tumor society
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• v.15 no.2
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• pp.130-137
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• 2009

Purpose: STAT3 is an oncogene that regulates critical cellular processes, and its constitutive activation has been demonstrated to correlate with biological and clinical features in many types of human malignancy. Materials and Methods: In this study, STAT3 activation was assessed in variable benign and malignant chondroid tumors in bone by immunohistochemistry using a monoclonal antibody specific for $tyrosine^{705}$-phosphorylated STAT3 ($pSTAT3^{tyr705}$). Results: Among conventional chondrosarcomas (n=17), three cases(50%) of grade III chondrosarcomas were pSTAT3-positive. All grade I and II chondrosarcomas were pSTAT3-negative. This pSTAT3 positivity according to the histologic grade was statistically significant (p=0.0432). Two cases(50%) of clear cell chondrosarcomas were pSTAT3-positive. Six cases (50%) among 12 benign chondroid tumors(6 enchondromas, 3 chondroblastomas, and 3 chondromyxoid fibromas) were also $pSTAT3^{tyr705}$-positive. Conclusion: In conclusion, STAT3 activation is associated with higher tumor grade in conventional chondrosarcomas. Our results suggest that STAT3 is activated in a subset of benign and malignant chondroid tumors, and may support the extension of the cancer stem cell hypothesis to include tumors of cartilaginous lineage.

• Clinical and Experimental Pediatrics
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• v.58 no.12
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• pp.472-477
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• 2015

Purpose: Adherence to treatment with inhaled corticosteroids (ICS) is a critical determinant of asthma control. The objective of this study was to assess factors that determine adherence to ICS therapy in children with asthma. Methods: Fifty-eight children with asthma, aged 5 to 16 years, used ICS with or without a spacer for 3 months. Adherence rates as measured from questionnaires and canisters, asthma symptom scores, and inhalation technique scores were assessed every 30 days. The degree of supervision by caregivers was assessed at day 30. Results: Adherence rates measured using canisters were lower at day 60 than at day 30 (P=0.044) and did not change thereafter ($74.4%{\pm}17.4%$ at day 30, $66.5%{\pm}18.4%$ at day 60, and $67.4%{\pm}22.2%$ at day 90). Adherence rates at days 60 and 90 and during the total study period were significantly different when measured by using questionnaires versus canisters (P<0.001, P=0.022, and P =0.001, respectively). In the comparison of adherence rates repeatedly measured at days 30, 60, and 90 and adherence rates during the total study period among the 3 groups, adherence rates in the high-degree supervision group were significantly higher than those in the low-degree supervision group ($82.0{\pm}16.0$ vs. $66.1{\pm}14.5$, $75.4{\pm}14.4$ vs. $56.2{\pm}18.4$, $75.0{\pm}18.3$ vs. $55.0{\pm}19.7$ [P=0.027]; $77.9{\pm}12.2$ vs. $59.1{\pm}11.4$ [P=0.021]) after adjustment for sex and age. Conclusion: The level of caregiver supervision is an important factor affecting adherence to ICS therapy in children with asthma. Therefore, a high degree of supervision may be required to increase adherence to ICS therapy in children with asthma.

• The Journal of Korean Society for Radiation Therapy
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• v.18 no.2
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• pp.119-125
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• 2006

Purpose: To measure the dose for dose optimization at the reference point (A, B) and the critical organ with multi Purpose brachytherapy phantom (MPBP). For this wort the MPBP was custom made, and designed to reconstruct the treatment applicator using multi function applicator (MFA) in the same way as the treatment of patient. Materials and Methods: Dose measurements were made at the reference points (A, B) and the bladder with thermoluminescence dosimeter (TLD) for four patients with tandem and ovoid of uterine cervix cancer using the phantom. In Phantom, Total 20 times of the measurements were made with 5 times a patient. Results: The results of TLD measurements in MPBP phantom showed the relative error ranging from -3.2% to 3.8% at A point, and -1.4% to 4% at B point and 1.3% to 7.15% at the bladder of reference point. Conclusion: The reproducibility of dose measurement under the same condition as the treatment could be achieved using the custom-made MFA in phantom and the dose at the reference point (A, B) and bladder could be analyzed accurately. The measured dose acquired in MPBP can apply for the dose optimization.

• Journal of the Korean Society of Food Science and Nutrition
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• v.41 no.9
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• pp.1226-1234
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• 2012

3,4,3',5'-Tetrahydroxy-trans-stilbene (piceatannol) is a derivative of resveratrol with a variety of biological activities, including anti-inflammatory, anti-proliferative, and anti-cancer activities. We assessed the mechanisms by which piceatannol inhibits inflammatory responses using lipopolysaccharide (LPS)-treated Raw264.7 murine macrophages. Piceatannol (0~10 ${\mu}mol/L$) decreased LPS-induced release of nitric oxide, tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-6, IL-$1{\beta}$, and inhibited LPS-induced protein expression of inducible nitric oxide synthase (iNOS). Activation of nuclear factor-kappaB (NF-${\kappa}B$), activator protein (AP)-1, and signal transducer and activator of transcription 3 (STAT3) are crucial steps during an inflammatory response. Piceatannol prevented LPS-induced degradation of inhibitor of ${\kappa}B$ ($I{\kappa}B$), translocation of p65 to the nucleus, and phosphorylation of stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK). Additionally, piceatannol inhibited LPS-induced phosphorylation of STAT3 and IL-6-induced translocation of STAT3 to the nucleus. Furthermore, piceatannol increased the protein and mRNA levels of hemeoxygenase (HO)-1, the rate-limiting enzyme of heme catabolism that plays a critical role in mediating antioxidant and anti-inflammatory effects. Piceatannol further induced antioxidant response elements (ARE)-driven luciferase activity in Raw264.7 cells transfected with an ARE-luciferase reporter construct containing the enhancer 2 and minimal promoter region of HO-1. These results suggest that piceatannol exerts anti-inflammatory effects via the down-regulation of iNOS expression and up-regulation of HO-1 expression.

• Molecules and Cells
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• v.40 no.9
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• pp.667-676
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• 2017

Abnormal differentiation of muscle is closely associated with aging (sarcopenia) and diseases such as cancer and type II diabetes. Thus, understanding the mechanisms that regulate muscle differentiation will be useful in the treatment and prevention of these conditions. Protein lysine acetylation and methylation are major post-translational modification mechanisms that regulate key cellular processes. In this study, to elucidate the relationship between myogenic differentiation and protein lysine acetylation/methylation, we performed a PCR array of enzymes related to protein lysine acetylation/methylation during C2C12 myoblast differentiation. Our results indicated that the expression pattern of HDAC11 was substantially increased during myoblast differentiation. Furthermore, ectopic expression of HDAC11 completely inhibited myoblast differentiation, concomitant with reduced expression of key myogenic transcription factors. However, the catalytically inactive mutant of HDAC11 (H142/143A) did not impede myoblast differentiation. In addition, wild-type HDAC11, but not the inactive HDAC11 mutant, suppressed MyoD-induced promoter activities of MEF2C and MYOG (Myogenin), and reduced histone acetylation near the E-boxes, the MyoD binding site, of the MEF2C and MYOG promoters. Collectively, our results indicate that HDAC11 would suppress myoblast differentiation via regulation of MyoD-dependent transcription. These findings suggest that HDAC11 is a novel critical target for controlling myoblast differentiation.

• Journal of Life Science
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• v.17 no.8 s.88
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• pp.1063-1067
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• 2007

The Bcl-2 family proteins play critical roles in regulation of apoptosis, and the balanced interaction of pro- and anti-death members is a key factor in determining the cell fate. Noxa, a BH3-only Bcl-2-family member, has been originally identified as a target gene of p53. To understand the mechanism by which human Noxa (hNoxa) regulates the cell death, we screened the hNoxa binding partner using the yeast two hybrid screening and found that anti-death protein Mcl-1 binds to hNoxa. The binding of hNoxa to Mcl-1 was confirmed by immunoprecipitation in human colon cancer cell line HCT 116 cells. Mcl-1 significantly inhibited the hNoxa-induced cell death in HCT 116 cells. During the cell death induced by hNoxa, Mcl-1 protein was degraded. Its degradation was inhibited by z-VAD-fmk, a pancaspase inhibitor, suggesting caspase is responsible for Mcl-1 degradation in response to hNoxa. Together, the results indicate that hNoxa binds to Mcl-1 that is degraded by cas-pases during hNoxa-induced cell death.