• Title/Summary/Keyword: anti-tumor drugs

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MULTIDISCIPLINARY APPROACH FOR THE DENTAL TREATMENT OF A PATIENT HAVING TRACHEOSTOMY TUBE (기관내삽관을 가진 장애환자의 치과치료를 위한 협의 진료)

  • Cha, Yoon-Sun;Kim, Ji-Hun
    • The Journal of Korea Assosiation for Disability and Oral Health
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    • v.10 no.1
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    • pp.38-42
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    • 2014
  • A tracheostomy tube serves as airway management for patients whose respiration is impeded due to inflammation, tumor, or traumatic events. If the patients who have tracheostomy tube, visit dental clinic for dental treatments, we should consider the underlying general condition of patients and then make treatment plans according to their state. A 22-Year old male patient, who had tracheostomy tube on his neck, came to our department for comprehensive dental treatment. Mild mental retardation was observed and he was taking anti-convulsant drugs for the prevention of epileptic seizure. Multiple advanced dental caries, hopeless teeth, and impacted third molars were also observed by clinical and radiographic examination. Due to the risk of epileptic seizure and low cooperativity to tolerate the treatment, general anesthesia was recommended by physician, and the anti-convulsant drug was administrated during procedure. In this case, we aimed to report the multidisciplinary approach for the dental treatment of patient having a tracheostomy tube.

Biological Activity and Inhibition of Non-Enzymatic Glycation by Methanolic Extract of Rosa davurica Pall. Roots

  • Hu, Weicheng;Han, Woong;Jiang, Yunyao;Wang, Myeong-Hyeon;Lee, Young-Mee
    • Preventive Nutrition and Food Science
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    • v.16 no.3
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    • pp.242-247
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    • 2011
  • The methanolic extract of Rosa davurica Pall. roots exhibited strong antioxidant activity in a 1,1-diphenyl-2-picryl-hydrazyl (DPPH) radical scavenging assay and was found to be a dose-dependent inhibitor of non-enzymatic formation of advanced glycation end products (AGEs), which are relevant to diabetes complications. HPLC-diode array detector (DAD) analysis of the R. davurica Pall. root extract led to the identification of four compounds: hydrocaffeic acid, catechin, epicatechin, and ellagic acid. Catechin was present in the largest amount and exhibited high antiglycation activity. A CYP3A4 assay was used to investigate potential interactions between drugs and the extract, and results suggest that the R. davurica Pall. root extract had moderate potential for interfering with drug metabolism. The R. davurica Pall. extract did not display anti-inflammatory activity on the level of that for tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in a lipopolysaccharide (LPS)-stimulated macrophage assay; however, the extract did exhibit low to moderate immunostimulatory activity in a pro-inflammatory macrophage assay. Therefore, we conclude that R. davurica Pall. root is a promising anti-AGE agent with low to moderate risks of associated inflammation or drug interaction.

The design for therapeutic agents of Leucine Rich Repeat protein using bioinformatics

  • Kim, Seong Yeol;Park, Beom Seok
    • International Journal of Advanced Culture Technology
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    • v.7 no.4
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    • pp.156-162
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    • 2019
  • Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by progressive joint deterioration; Furthermore, RA can also affect body tissues, including the skin, eyes, lungs, heart and blood vessels. The early stages of RA can be difficult to diagnose because the signs and symptoms mimic those of many other diseases. It is not known exactly what triggers the onset of RA and how to cure the disease. But recent discoveries indicate that remission of symptoms is more likely when treatment begins early with strong medications known as disease-modifying anti-rheumatic drugs (DMARDs). Tumor necrosis factor (TNF) inhibitors are typical examples of biotherapies that have been developed for RA. The substances may occur naturally in the body or may be made in the laboratory. Other biological therapies care biological response modifiers (BRMs)such as monoclonal antibodies, interferon, interleukin-2 (IL-2) and a protein binder using repeat units. These substances play significant anti-inflammatory roles. Proteins with recurrent, conserved amino acid stretches mediate interactions among proteins for essential biological functions; for example, ankyrin (ANK), Heat repeat protein (HEAT), armadillo repeat protein (ARM) and tetratricopeptide repeats (TPR). Here, we describe Leucine rich repeats (LRR) that ideally fold together to form a solenoid protein domain and is more applicable to our current study than the previously mentioned examples. Although BRMs have limitations in terms of immunogenicity and effector functions, among other factors, in the context therapeutic use and for proteomics research, We has become clear that repeat-unit-derived binding proteins will increasingly be used in biotechnology and medicine.

Anti-apoptotic Effect of Bojungbangam-tang Ethanol Extract on Cisplatin-Induced Apoptosis in Rat Mesangial Cells

  • Kim, Nam-Su;Ju, Sung-Min;Kwon, Young-Dal;Shin, Byung-Cheul;Ahn, Kyoo-Seok;Kim, Sung-Hoon;Song, Yung-Sun;Jeon, Byung-Hun
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.6
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    • pp.1664-1671
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    • 2006
  • Cisplatin is a anti-neoplastic agent which is commonly used for the treatment of solid tumor. Cisplatin activates multiple signal transduction pathways involved in the stress-induced apoptosis in a variety of cell types. Cytotoxicity of cisplatin was detected in rat mesangial cells and the value of $IC_{50}$ is about 20 ${\mu}M$. The treatment of cisplatin to rat mesangial cells showed the apoptotic bodies and DNA fragmentation. The activation of caspase-3, -8, and -9 and proteolytic cleavage of PARP were observed in the rat mesangial cells treated time-dependently with cisplatin. The activation of ERK, p38 and JNK was also observed in the apoptosis induced by cisplatin in rat mesangial cells. The ethanol extract of Bojungbangam-tang (EBJT), a new hergal prescription composed of nine crude drugs, inhibited cisplatin-induced apoptosis in rat mesangial cells. EBJT reduced sub-G1 peak (apoptotic peak) in cisplatin-treated rat mesangial cells. The cisplatin-induced ERK and JNK activation in rat mesangial cells were blocked by EBJT, but EBJT had no effect on p38 activation. Taken together, these results con suggest that EBJT prevents cisplatin-induced apoptotic cell death in rat mesangial cells through inhibition of ERK and JNK activation.

Inducing Apoptosis of NCI-H157 Human Lung Carcinoma Cells via Activation of Caspase Cascade by Combination Treatment with Arsenic Trioxide and Sulindac (NCI-H157 폐암 세포주에서 Caspase Cascade 활성을 통한 Arsenic Trioxide와 Sulindac 병합요법의 세포고사효과)

  • Kim, Hak Ryul;Yang, Sei Hoon;Jeong, Eun Taik
    • Tuberculosis and Respiratory Diseases
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    • v.56 no.4
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    • pp.381-392
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    • 2004
  • Arsenic trioxide($As_2O_3$) was introduced into the treatment of refractory or relapsed acute promyelocytic Ieukemia. Some investigators have reported that arsenic trioxide had induced apoptosis in a variety of solid human tumor cell lines, including non-small cell lung cancer. Non-steroidal anti-inflammatory drugs(NSAIDs) are powerful chemopreventive agents for gastrointestinal cancers and the growth of established tumors are reduced by inducing apoptosis. It's also reported that NSAIDs enhanced tumor response to chemotherapeutic drugs or radiation. In this study, we aimed to determine whether combination of arsenic trioxide with sulindac augmented its apoptotic potential in NCI-H157 human lung cancer cells. The human lung cancer cell line NCI-H157 was treated with arsenic trioxide and sulindac. Cell viability was measured by the MTT assay. Apoptosis was measured by nuclear staining and flow cytometric analysis. The catalytic activity of the caspase families were measured by the fluorogenic cleavage of biosubstrates. The western blotting were also performed to define the mechanical basis of apoptosis. Combination treatment of arsenic trioxide and sulindac decreased the viability of NCI-H157 human lung cancer cells in a dose-dependent manner. The catalytic activity of caspase-3, 8 and 9 proteases were increased after combination treatment. Consistently PARP was cleaved from 116kDa to 85kDa fragments, and the expression of ICAD was decreased by time-dependent manner. Also combination treatment increased the expression of Fas and Fas/L. Combination therapy of arsenic trioxide with sulindac augments cell death and induces apoptosis via the activation of caspase cascade in NCI-H157 human lung carcinoma cells.

Effect of the Hexane Extract of Saussurea lappa on the Growth of HT-29 Human Colon Cancer Cells (목향 헥산추출물이 대장암세포인 HT-29 세포의 증식에 미치는 영향)

  • Kim, Eun-Ji;Park, Hee-Sook;Lim, Soon-Sung;Kim, Jong-Sang;Shin, Hyun-Kyung;Yoon, Jung-Han
    • Korean Journal of Food Science and Technology
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    • v.40 no.2
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    • pp.207-214
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    • 2008
  • In Asia Saussurea lappa (SL) has been used as a traditional herbal medicine to treat abdominal pain and tenesmus. Recently, in vitro cell culture studies have shown that SL has anti-ulcer, anti-inflammatory, and anti-tumor properties. To explore its potential chemopreventive and chemotherapeutic effects in colon cancer, we examined whether the hexane extract of SL (HESL) could inhibit the growth of HT-29 human colon cancer cells, and investigated the mechanisms for this effect. The cells were cultured with various concentrations (0-5 ${\mu}g/mL$) of HESL. The results indicated that HESL markedly decreased the numbers of viable HT-29 cells; whereas at the concentration of 5 ${\mu}g/mL$, HESL slightly decreased the viable cell numbers of CCD 1108Sk human skin normal fibroblasts at 72 hr. HESL substantially increased the numbers of cells in the sub G1 phase, and dose-dependently increased apoptotic cell numbers. Western blot analysis of the total cell lysates revealed that HESL increased Bax protein levels, but did not affect Bcl-2 levels. HESL induced the cleavage of poly (ADP-ribose) polymerase and caspases 8, 9, 7, and 3. This study demonstrated that HESL inhibits cell growth and induces apoptosis in HT-29 cells, which may be mediated by its ability to increase Bax levels and activate the caspase pathway. These findings may lead to the development of new therapeutic strategies for colon cancer treatment.

Effect of ZNimesulide on the Differentiation and Survival of Endothelial Progenitor Cells

  • Oh, Ho-Kyun;Kim, Sun-Yong;Baek, Sang-Hong;Lim, Sung-Cil;Ahn, Hyun-Young;Shin, Jong-Chul;Hong, Sung-Hee;Hong, Yong-Kil;Joe, Young-Ae
    • Biomolecules & Therapeutics
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    • v.12 no.4
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    • pp.221-227
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    • 2004
  • Nonsteroidal anti-inflammatory drugs (NSAIDs), particularly the highly selective cyclooxygenase (COX)-2 inhibitors have been shown to decrease the growth of tumor, in part, by inhibition of neovascularization. Recently, besides mature endothelial cells, endothelial progenitor cells (EPCs) have been shown to contribute neovascularization in angiogenic tissues. In this study, we addressed a question whether nimesulide, a selective COX-2 inhibitor, could affect differentiation of EPCs into adhesive endothelial cells in vitro. Total mononuclear cells were isolated from cord blood by Ficoll density gradient centrifugation, and then the cells were incubated with nimesulide or vehicle control for 7 days. The number of adherent and spindle-shaped cells decreased by nimesulide treatment in a concentration-dependent fashion at a concentration range of 5 - 200 ${\mu}M$. Moreover, the adherent cells double positive for DiI-ac-LDL uptake and lectin binding significantly decreased upon nimesulide treatment. There was no change of expression of CD31 between treatment and control groups, whereas slight reduction was detected upon treatment in expression of VE-cadherin, ICAM-1, vWF, ${\alpha}v$, and ${\alpha}5$. Nimesulide also reduced cell viability during first 3 days' culture and induced apoptosis in adherent EPCs, resulting in increased annexin-V-positive and propidium iodide-negative cells. Taken together, these results suggest that nimesulide could be applied for the inhibition of new vessel formation, in part, by inhibiting differentiation and survival of EPCs.

Prognostic Significance of Cyclooxygenase-2(COX-2) Expression in Primary, Resected Non-Small Cell Lung Cancer (원발성 비소세포폐암조직에서 Cyclooxygenase-2 발현의 예후인자로서의 의의)

  • Kim, Hak Ryul;Yang, Sei Hoon;Jeong, Eun Taik
    • Tuberculosis and Respiratory Diseases
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    • v.56 no.2
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    • pp.169-177
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    • 2004
  • Background : Cyclooxygenase is the main target enzyme for the nonsteroidal anti inflammatory drugs (NSAIDs) that have been shown to suppress carcinogenesis in both experimental models and epidemiological studies. COX-2 plays an important role in solid tumor growth, invasiveness and angiogenesis, through, in part, the synthesis of prostaglandins, such as prostaglandin E2 (PGE2). In this study, the prognostic significance of an increase in COX-2 expression in lung cancer samples was evaluated. Material and Methods : The expression of COX-2, by immunohistochemistry, was studied in paraffin-embedded tumor blocks obtained from 84 patients(male 67, female 17, with a mean age of 63, ranging from 34 to 84 years) who had undergone surgery at Wonkwang University Hospital, between 1997 and 2002. For the evaluation of the relationships between COX-2 expression, and the clinical stage, metastasis to lymph nodes and survival, those cases showing the respective antigen expression in >10% of the tumor cells were considered positive. Result : Of the 84 patients, 61 (73%) exhibited more than 10% COX-2 immunoreactivities in the tumor and normal cells, whereas the remaining 23 showed no increase in the expression of COX-2. There was no significant relationship between the increased expression of COX-2 and the disease stage(p=0.1002) or cell type(p=0.152). The median survival was longer for the patients with a negative, compared to positive, COX-2 expression(36 compared to 24 months, p<0.05). The two year-survival rate was also higher in the patients with a negative COX-2 expression (78%) than those with a positive expression (47%, Kaplan-Meier, Log Rank, p < 0.05). Conclusion : The median survival was longer in the patients with a negative, compared to positive, COX-2 expression was longer than those with positive COX-2, having undergone complete resection due to primary non-small cell lung cancer.

Phloroglucinol Inhibits the in vitro Differentiation Potential of CD34 Positive Cells into Endothelial Progenitor Cells

  • Kwon, Yi-Hong;Lee, Jun-Hee;Jung, Seok-Yun;Kim, Jae-Won;Lee, Sang-Hun;Lee, Dong-Hyung;Lee, Kyu-Sup;Lee, Boo-Yong;Kwon, Sang-Mo
    • Biomolecules & Therapeutics
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    • v.20 no.2
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    • pp.158-164
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    • 2012
  • Inhibiting the bioactivities of circulating endothelial progenitor cells (EPCs) results in significant inhibition of neovessel formation during tumor angiogenesis. To investigate the potential effect of phloroglucinol as an EPC inhibitor, we performed several in vitro functional assays using $CD34^+$ cells isolated from human umbilical cord blood (HUCB). Although a high treatment dose of phloroglucinol did not show any cell toxicity, it specifically induced the cell death of EPCs under serum free conditions through apoptosis. In the EPC colony-forming assay (EPC-CFA), we observed a significant decreased in the small EPC-CFUs for the phloroglucinol group, implying that phloroglucinol inhibited the early stage of EPC commitment. In addition, in the in vitro expansion assay using $CD34^+$ cells, treatment with phloroglucinol was shown to inhibit endothelial lineage commitment, as demonstrated by the decrease in endothelial surface markers of EPCs including $CD34^+$, $CD34^+/CD133^+$, $CD34^+/CD31^+$ and $CD34^+/CXCR4^+$. This is the first report to demonstrate that phloroglucinol can inhibit the functional bioactivities of EPCs, indicating that phloroglucinol may be used as an EPC inhibitor in the development of biosafe anti-tumor drugs that target tumor angiogenesis.

Antimetastatic and Antitumor Effect of Ginsenoside Rh2 and ${\beta}-glucan$ in Mice (Ginseniside Rh2와 베타 글루칸의 암세포 전이억제효과)

  • Lee, Chang-Hwan;Won, Eun-Kyung;Sung, Hyun-Jea;Choung, Se-Young
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.21 no.4
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    • pp.856-859
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    • 2007
  • We have investigated the antimetastatic and antitumor effects of Ginsenoside Rh2 and ${\beta}-glucan$ unsing an experimental metastatic mouse model intravenously injected with B 16 melanoma F 10 cells. Animal groups are divided into six groups according to the dosage of drug administration and the kind of drugs. The groups are control, ${\beta}-glucan$ with 50, 100 and 200 mg/kg, Geinsenoside Rh2 50 mg/kg, and ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg. Oral administration of various concentration of ${\beta}-glucan$( 50, 100, and 200 mg/kg) were reduced the lung- metastatics induced by metastatic B16 melanoma F 10 cells injection with a dose dependent manner in the syngenic mice. At same dosage group, Ginsenoside Rh2 (50 mg/kg) has more antimetastatic effect than the ${\beta}-glucan$(50 mg/kg). The highest antimetastatic effects was observed in the ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg group and has a similar tendency in the anti-tumor effects, including decrease of the average tumor weight and increase of the average survival rate. There are no differences of the average tumor weights were apparent in the ${\beta}-glucan$ groups, however there were little decrease of the average tumor weight in Ginsenoside 50 mg/kg group and ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg group than that of the control group. The rate of average survival rate in the ${\beta}-glucan$ 50 mg/kg + Ginsenoside Rh2 50 mg/kg group, ${\beta}-glucan$ 200 mg/kg, ${\beta}-glucan$ 100 mg/kg and ${\beta}-glucan$ 50 mg/kg, and Ginsenoside 50 mg/kg groups were highly in order. These data suggest that antimetastatic and antitumor effect of combination of Ginsenodide Rh2 and ${\beta}-glucan$ be the highest in this study.