• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.29 no.2
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• pp.108-115
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• 2003

Suppression of cellular immunity is the host responses to surgical stress. When the body is exposed to surgical stress, decreased immunocyte function is one of the surgical stress-induced biologic responses. In all patients exposed to the surgical stress, peripheral blood lymphocyte numbers and function were suppressed until at least 2 weeks postoperatively. This immunosuppression was mainly due to a decrease of helper-inducer T cells, cytotoxic T cells, natural killer cells, and an increase of suppressor T cells. The blood levels of interleukin-6(IL-6) cytokine increase in response to surgical stress and cause an increase of so-called acute phase reactants, including C-reactive protein(CRP). In the previously damaged patients group, expected to early stress expose, immunosuppression was more developed than other normal groups. Cellular immunosuppression by surgical stress was mainly due to an increase of lymphocyte subsets that depress cellular immunity coupled with a decrease of the subsets that promote it. Overproduction of CRP in response to surgical stress may play an important role in the development of immunosuppression.

• 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.16 no.6
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• pp.1122-1126
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• 2002

We have examined whether Soamsan 1 (SA 1) augment the inhibitory effect of oral administration of Soamsan (SA) on lung metastasis of mouse 816 melanoma cells. The inhibitory effect was slightly enhanced by increase in administration dosage of SA 1. SA 1 as well as SA inhibited effectively the lung metastasis regardless of the pretreatment with anti-mouseNK monoclonal antibody. However, in the case of 2-chloroadenosine-pretreated mice, the inhibitory effects of SA and SA 1 were decreased by 18 and 23%, respectively. In vitro stimulation of the mouse splenocytes with mitogens showed that SA or SA 1 significantly augmented the proliferation of mouse splenocytes. Especially, the activity was more prominent in the presence of a B cell mitogen. LPS than a T cell mitogen, Con A. These results suggest that oral administration of SA 1 or SA inhibited lung metastasis of B16 melanoma cells, possibly through a mechanism mediated by the activation of macrophages and B lymphocytes in the host immune system. However, SA 1 did not showed more significant augment of the activation of immune system than SA.

• The Plant Pathology Journal
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• v.25 no.2
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• pp.113-120
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• 2009

Microscopic study of chili pepper (Capsicum annuum L.) infected with Phytophthora capsici, causing Phytophthora blight of chili pepper, was conducted to compare histological and cytological characteristics in the root and stem of susceptible (C. annuum cv. Bugang) and resistant (C. annuum cv. CM334) pepper cultivars. The susceptible pepper roots and stems were extensively penetrated and invaded by the pathogen initially into epidermal cells and later cortical and vascular cells. Host cell walls adjacent to and invaded by the infecting hyphae were partially dissolved and structurally loosened with fine fibrillar materials probably by cell wall-degrading enzymes of the pathogen. In the resistant pepper, the pathogen remained on root epidermal surface at one day after inoculation, embedded and captured in root exudation materials composed of proteins and polysaccharides. Also the pathogen appeared to be blocked in its progression at the early infection stages by thickened middle lamellae. At 3 days after inoculation, the oomycete hyphae were still confined to epidermal cells of the root and at most outer peripheral cortical cells of the stem, resulting from their invasion blocked by wound periderms formed underneath the infection sites and/or cell wall appositions bounding the hyphal protrusions. All of these aspects suggest that limitation of disease development in the resistant pepper may be due to the inhibition of the pathogen penetration, infection, invasion, and colonization by the defense structures such as root exudation materials, thickened middle lamellae, wound peridems and cell wall appositions.

• Journal of Oral Medicine and Pain
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• v.40 no.2
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• pp.82-87
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• 2015

Methotrexate (MTX) is a chemotherapeutic agent that is used to treat a host of malignancies. But recently, MTX has also been used as a therapeutic agent for chronic inflammatory disorders such as rheumatoid arthritis, psoriasis, and systemic lupus erythematosus. However, MTX is an antimetabolite that affects rapidly dividing normal cells such as oral mucosal epithelial cells, gastrointestinal epithelial cells, and bone marrow cells-which explains why oral mucositis is often an initial manifestation of MTX toxicity. Because oral lesions are frequently initially presented in dental clinics, dentists should consider the possibility of adverse drug reactions in the differential diagnoses of oral lesions through a meticulous collection of patients' medical histories. In this report, we examine patients who suffered from oral ulcerative lesions upon diagnosis of MTX-induced oral mucositis. Then, we suggest approaches for the diagnosis and treatment of MTX-induced oral mucositis through a review of literature.

• BMB Reports
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• v.49 no.5
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• pp.263-269
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• 2016

The intestine represents the largest and most elaborate immune system organ, in which dynamic and reciprocal interplay among numerous immune and epithelial cells, commensal microbiota, and external antigens contributes to establishing both homeostatic and pathologic conditions. The mechanisms that sustain gut homeostasis are pivotal in maintaining gut health in the harsh environment of the gut lumen. Intestinal epithelial cells are critical players in creating the mucosal platform for interplay between host immune cells and luminal stress inducers. Thus, knowledge of the epithelial interface between immune cells and the luminal environment is a prerequisite for a better understanding of gut homeostasis and pathophysiologies such as inflammation. In this review, we explore the importance of the epithelium in limiting or promoting gut inflammation (e.g., inflammatory bowel disease). We also introduce recent findings on how small RNAs such as microRNAs orchestrate pathophysiologic gene regulation.

• Journal of Microbiology and Biotechnology
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• v.14 no.1
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• pp.121-127
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• 2004

Amphotericin B (AmB), an amphipathic polyene macrolide, is an antifungal drug produced by Streptomyces nodosus. Recently, AmB has been shown to exert antiviral activity against rubella virus and human immunodeficiency virus by different mechanisms. In this study, we evaluated the antiviral effect of AmB against Japanese encephalitis virus (JEV) and investigated which step of the viral life cycle was inhibited by AmB to understand the mechanism of antiviral action of AmB. AmB reduced both plaque size and number in the infected cells in a dose-dependent manner. In addition, a 200-fold reduction of infectious virus titer was observed by treatment of infected cells with $5\mug/ml$ of AmB. AmB acted at the post virus-infection step, but not during adsorption of virus to host cells. Western blot analysis revealed that the accumulated level of JEV envelope protein dramatically decreased in the infected cells by treatment with $5-10\mug/ml$ of AmB. Our results indicate that AmB inhibits the replication of JEV at the postinfection step by interfering with viral replication and/or by inhibiting the synthesis of viral proteins.

• Journal of Periodontal and Implant Science
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• v.41 no.3
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• pp.157-163
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• 2011

Purpose: Curcumin is known to exert numerous biological effects including anti-inflammatory activity. In this study, we investigated the effects of curcumin on the production of interleukin-6 (IL-6) by murine macrophage-like RAW 264.7 cells stimulated with lipopolysaccharide (LPS) from Prevotella intermedia, a major cause of inflammatory periodontal disease, and sought to determine the underlying mechanisms of action. Methods: LPS was prepared from lyophilized P. intermedia ATCC 25611 cells by the standard hot phenol-water method. Culture supernatants were collected and assayed for IL-6. We used real-time polymerase chain reaction to detect IL-6 mRNA expression. $I{\kappa}B-{\alpha}$ degradation, nuclear translocation of NF-${\kappa}B$ subunits, and STAT1 phosphorylation were characterized via immunoblotting. DNA-binding of NF-${\kappa}B$ was also analyzed. Results: Curcumin strongly suppressed the production of IL-6 at both gene transcription and translation levels in P. intermedia LPS-activated RAW 264.7 cells. Curcumin did not inhibit the degradation of $I{\kappa}B-{\alpha}$ induced by P. intermedia LPS. Curcumin blocked NF-${\kappa}B$ signaling through the inhibition of nuclear translocation of NF-${\kappa}B$ p50 subunit. Curcumin also attenuated DNA binding activity of p50 and p65 subunits and suppressed STAT1 phosphorylation. Conclusions: Although further study is required to explore the detailed mechanism of action, curcumin may contribute to blockade of the host-destructive processes mediated by IL-6 and appears to have potential therapeutic values in the treatment of inflammatory periodontal disease.

• 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.

• Journal of Microbiology
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• v.38 no.4
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• pp.270-274
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• 2000

Pathogenic Salmonella typhimurium can invade the intestinal epithelium and cause a wide range of diseases including gastroenteritis and bacteremia in human and animals. To identify the genes involved in the infection, the invasion determinant was obtained from S. typhimurium 82/6915 and was subcloned into pGEM-7Z. A subclone DHl (pSV6235) invaded HEp-2 and Chinese hamster ovary epithelial cells and contained a 4.4 kb fragment of S. typhimurium genomic region. Compared with the host strain E. coli DHl, the subclone DHl (pSV6235) invaded cultured HEp-2 and Chinese hamster ovary cells at least 75- and 68-fold higher, respectively. The invasion rate of E. coli DHl for the cells significantly increased by harbouring the genomic region derived from pathogenic S. typhimurium 82/6915.