• BMB Reports
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• v.51 no.5
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• pp.219-224
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• 2018

Necroptosis is an emerging form of programmed cell death occurring via active and well-regulated necrosis, distinct from apoptosis morphologically, and biochemically. Necroptosis is mainly unmasked when apoptosis is compromised in response to tumor necrosis factor alpha. Unlike apoptotic cells, which are cleared by macrophages or neighboring cells, necrotic cells release danger signals, triggering inflammation, and exacerbating tissue damage. Evidence increasingly suggests that programmed necrosis is not only associated with pathophysiology of disease, but also induces innate immune response to viral infection. Therefore, necroptotic cell death plays both physiological and pathological roles. Physiologically, necroptosis induce an innate immune response as well as premature assembly of viral particles in cells infected with virus that abrogates host apoptotic machinery. On the other hand, necroptosis per se is detrimental, causing various diseases such as sepsis, neurodegenerative diseases and ischemic reperfusion injury. This review discusses the signaling pathways leading to necroptosis, associated necroptotic proteins with target-specific inhibitors and diseases involved. Several studies currently focus on protective approaches to inhibiting necroptotic cell death. In cancer biology, however, anticancer drug resistance severely hampers the efficacy of chemotherapy based on apoptosis. Pharmacological switch of cell death finds therapeutic application in drug- resistant cancers. Therefore, the possible clinical role of necroptosis in cancer control will be discussed in brief.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.3
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• pp.777-779
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• 2003

Among extracts prepared from Alstonia scholaris, Phyllostachys pubescens and Bambusa veitchii, methanol fraction of Alstonia scholaris was found to have antiplasmodial effect by inhibiting growth of the chloroquine-resistant Plasmodium falciparum strain FCR-3 with less than 14 μg/ml of EC50 values. Methanol fraction 2 of Alstonia scholaris revealed the strongest anti plasmodial effect with 40 μg/ml of EC50 value. Especially, this fraction showed higher than 3-folds selective toxicity on a Plasmodium as the EC value was 116 μg/ml on the host FM3A cell. This is the first report on which an extract compound from Alstonia scholaris showed antimalarial effect.

• Proceedings of the Korean Society of Plant Pathology Conference
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• 2005.10a
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• pp.15-20
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• 2005

Locations of silicon accumulation in rice leaves and its possible association with resistance to rice blast were investigated by analytical electron microscopy and atomic force microscopy. A blast-susceptible cultivar, Jinmi, and partially resistant cultivars, Hwaseong and Suwon345, were grown under a hydroponic culture system with modified Yoshida's nutrient solution. Electron-dense silicon layers were frequently found beneath the cuticle in epidermal cell walls of silicon-treated plants. Increasing levels of silicon were detected in the outer regions of epidermal cell walls. Silicon was present mainly in epidermal cell walls, middle lamella, and Intercellular spaces within subepidermal tissues. Furthermore, silicon was prevalent throughout the leaf surface with relatively small deposition on stomatal guard cells in silicon-treated plants. Force-distance curve measurements revealed relative hardness and smaller adhesion force in silicon-treated plants (18.65 uN) than control plants (28.39 uN). Moreover, force modulation microscopy showed higher mean height values of elastic Images In silicon-treated plants(1.26 V) than in control plants (0.44 V), implying the increased leaf hardness by silicon treatment. These results strongly suggest that silicon-induced cell wall fortification of rice leaves may be closely associated with enhanced host resistance to blast.

• The Plant Pathology Journal
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• v.17 no.3
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• pp.128-140
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• 2001

Infection of pepper leaves by Colletotrichum cocodes at the two- and eight-leaf stages caused susceptible and resistant lesions 96 h after inoculation, respectively. At the two-leaf stage, progressive symptom development occurred on the infected leaves. In contrast, localized necrotic spots were characteristic symptoms at the eight-leaf stage. Infected leaves at the two-leaf stage exhibited cell death accompanied by the accumulation of autofluorescent compounds. At the eight-leaf stage, pepper leaves infected by the anthracnose fungus displayed localized autofluorescence from the symptoms. Infection of pepper leaves by C. cocodes at the two-leaf stage resulted in its rapidand massive colonization of all the leaf tissues including the vascular tissue, together with cytoplasmic collapse, distortion of chloroplasts, and disruption of host cell walls. However, penetration of C. cocodes was very limited in the older leaf tissues of pepper plants at the eight-leaf stage. Fungal hyphae grew only in the intramural spaces of the epidermal cell walls at this stage. Occlusion of amorphous material in xylem vessels, aggregation of fibrillar material in inter-cellular spaces, and deposition of protein bodies were found as resistance responses to C. cocodes.

• Journal of Microbiology and Biotechnology
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• v.28 no.8
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• pp.1270-1281
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• 2018

Periodontal disease is triggered by the host immune response to pathogens in the microbial biofilm. Worsening of periodontal disease destroys the tooth-supporting tissues and alveolar bone. As oral inflammation can induce systemic diseases in humans, it is important to prevent periodontal disease. In this study, we demonstrated that Curcuma xanthorrhiza supercritical extract (CXS) and its active compound, xanthorrhizol (XAN), exhibit anti-inflammatory effects on lipopolysaccharide (LPS)-treated human gingival fibroblast-1 cells and anti-osteoclastic effects on receptor activator of nuclear factor kappa B ligand (RANKL)-treated RAW264.7 cells. LPS-upregulated inflammatory factors, such as nuclear factor kappa B p65 and $interleukin-1{\beta}$, were prominently reduced by CXS and XAN. In addition, RANKL-induced osteoclastic factors, such as nuclear factor of activated T-cells c1, tartrate-resistant acid phosphatase, and cathepsin K, were decreased in the presence of CXS and XAN. CXS and XAN inhibited the mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) signaling pathway. Collectively, these results provide evidence that CXS and XAN suppress LPS-induced inflammation and RANKL-induced osteoclastogenesis by suppressing the MAPK/AP-1 pathway.

• Korean Journal of Veterinary Service
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• v.37 no.1
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• pp.35-43
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• 2014

Salmonellosis has caused heavy losses in swine industry and implications for public health. Recently, the urgent problem of antibiotic resistance due to multidrug-resistant Salmonella spp. has been on the rise. The use of host-specific bateriophages as a biocontrol is one possible alternative. In this study, clinical signs, growth performance, quantification and detection of antigen, histopathological changes of gastrointestinal tracts were analyzed comparatively in weaned piglets according to administration of bacteriophages and challenge with Salmonella (S.) Typhimurium. Piglets challenged with S. Typhimurium after administered with bacteriophages showed reduced clinical signs, higher growth performance, lower bacterial shedding, lower quantificational value of antigens in intestines, higher V/C ratio and higher the number of goblet cells in intestines than piglets administered without bacteriophage and challenged with S. Typhimurium. These results indicate that feeding contained with bacteriophages has effect to prevent infection of S. Typhimurium in weaned piglets and suggest that a use of bacteriophage can be considered a valid antibiotic alternative.

• Journal of Periodontal and Implant Science
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• v.30 no.4
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• pp.725-736
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• 2000

It is becoming increasingly apparent that periodontitis consists of mixture of diseases, most of which respond favorably to traditional mechanical therapy. Among these variants of the disease, some appear to be associated with unusual microbial infections and defective host defenses. Many of these fail to respond to conventional treatment. The recognition that some forms of periodontitis are refractory to standard periodontal therapy has given rise to a new classification of peridontitis. A series of 1692 subgingival microbial samples sent to a diagnostic microbiology laboratory included 738 samples that could be identified as compatible with a clinical diagnosis of refractory or recurrent periodontitis. In descending order of prevalence the associated microbiota included Bacteroides forsythus(85%) ,Fusobacterium species(78%), Spirochetes(67%), Campylobacter rectus(64%), Porphyromonas gingivalis(59%), Peptostreptococcus micros(58%), motile rods(46%), Prevotella intermedia(33%), Eikenella corrodens(13%), Capnocytophaga species(12%) ,and Actinobacillus actinomycetemcomitans(6%). Antibiotic resistance to tetracycline, penicillin G, or metronidazole was particularly noticeable for Fusobacterium species, Capnocytophaga species, and Actinobacillus actinomycetemcomitans. It was largely absent for Campylobacter rectus. No antibiotic data were obtained for Porphyromonas gingivalis or Bacteroides forsythus, as these species were detected by immunofluorescence. The results indicate that a substantial number of microorganisms associated with refractory periodontitis are variably resistant to commonly-used antibiotics. Diagnostic microbiology must be considered an essential adjunct to the therapist faced with periodontal lesions refractory to conventional treatment.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.27 no.2
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• pp.110-122
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• 2005

Adenoid cystic carcinoma (ACC) of salivary glands has a protracted clinical course with perineural invasion, delayed onset of hematogenous metastasis, and poor responses to classical cytotoxic chemotherapic agents. Most deaths from salivary ACC are caused by lung metastases that are resistant to conventional therapy. Therefore, knowledge of cellular properties and tumor-host interactions that influence the dissemination of metastatic cells is important for the design of more effective therapy of salivary cancer. I determined in vitro expression of epidermal growth factor receptor (EGFR) and its downstream effectors and vascular endothelial growth factor receptor (VEGFR)-2 on a human salivary ACC cell line (ACC2). I also evaluated the expression of EGF and VEGF signaling molecules and metastasis-related proteins on human salivary ACC cells orthotopically growing in nude mice. In Western blot and immunohistochemical analyses, EGFR and VEGFR-2 were presented and phosphorylated in ACC2 cells. In human parotid cancer xenografts in nude mice, EGF and VEGF signaling molecules, IL-8, and MMP-9 were expressed at markedly higher levels than in normal parotid tissues. Moreover, tumor-associated endothelial cells of this orthotopic parotid tumor expressed phosphorylated VEGFR-2 and phosphorylated Akt, which is a cell-survival protein. These data show that those biomarkers can be molecular targets for therapy of salivary ACC, which has a propensity for delayed lung metastasis.

• The Journal of the Acoustical Society of Korea
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• v.20 no.2
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• pp.66-76
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• 2001

Conventional echo watermarking techniques often exhibit inherent trade-offs between imperceptibility and robustness. In this paper, a new echo embedding technique is proposed. The proposed method enables one to embed high energy echoes while the host audio quality is not deteriorated, so that it is robust to common signal processing modifications and resistant to tampering. It is possible due to echo kernels that are designed based on psychoacoustic analyses. In addition, we propose some novel techniques to improve robustness against signal processing attacks. Subjective and objective evaluations confirmed that the proposed method could improve the robustness without perceptible distortion.

• Journal of Microbiology and Biotechnology
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• v.26 no.8
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• pp.1490-1503
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• 2016

Colorectal cancer (CRC) is the third most common cancer in the world. Although 5-fluorouracil (5-FU) is the representative chemotherapy drug for colorectal cancer, it has therapeutic limits due to its chemoresistant characteristics. Colorectal cancer cells can develop into cancer stem cells (CSCs) with self-renewal potential, thereby causing malignant tumors. The human gastrointestinal tract contains a complex gut microbiota that is essential for the host's homeostasis. Recently, many studies have reported correlations between gut flora and the onset, progression, and treatment of CRC. The present study confirms that the most representative symbiotic bacteria in humans, Lactobacillus plantarum (LP) supernatant (SN), selectively inhibit the characteristics of 5-FU-resistant colorectal cancer cells (HT-29 and HCT-116). LP SN inhibited the expression of the specific markers CD44, 133, 166, and ALDH1 of CSCs. The combination therapy of LP SN and 5-FU inhibited the survival of CRCs and led to cell death by inducing caspase-3 activity. The combination therapy of LP SN and 5-FU induced an anticancer mechanism by inactivating the Wnt/β-catenin signaling of chemoresistant CRC cells, and reducing the formation and size of colonospheres. In conclusion, our results show that LP SN can enhance the therapeutic effect of 5-FU for colon cancer, and reduce colorectal cancer stem-like cells by reversing the development of resistance to anticancer drugs. This implies that probiotic substances may be useful therapeutic alternatives as biotherapeutics for chemoresistant CRC.