• The korean journal of orthodontics
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• v.26 no.2 s.55
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• pp.187-196
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• 1996

Underlying malocclusions and dentofacial deformities are often related to variations in the craniofacial development. Type I and type II collagens are considered the major collagens of bone and cartilage respectively. Monitoring the patterns of those protein expressions during development will Provide a basis for the understanding of normal and abnormal growths. This study was undertaken to investigate the morphogenetic changes and the expression patterns of type I and II collagen proteins involved in the developing mandible of human embryos and fetuses. 50 embryos and fetuses were studied with Hematoxylin and Eosin, Alcian, blue-PAS, Masson Trichrome, md Immunohistochemical stains. The results were as follows : 1. A 13.5 mm embryo showed the stomatodeum with dental lamina, maxillary and mandibular processes. Meckel's cartilage appeared in the mandibular arch of a 20.5 mm embryo. New bone formation was bilaterally initiated at the outer side of middle portion of Meckel's cartilage of 22-38 mm embryos. 2. Meckel'cartilage was resorbed at the 15th week fetus. The endochondral ossification was observed where there was direct replacement of cartilage by bone. Meckel'cartilage disappeared and membraneous ossification were observed at the 25th week. 3. Before the appearance of Meckel's cartilage, the expression of type I collagen was moderate at the odontogenic epithelium of maxillary & mandibular process, but mild for the expression of type II collagen. 4. During the appearance of Meckel's cartilage and new bone formation, the immunoactivity of type II collagen was more expressed than type I collagen at the Meckel's cartilage and new bone. 5. During intrarmembranous bone formation, the expression of type II collagen was rare in the bony trabeculae. There was a switch for the expression of collagens from type II to type I during the appearance of Meckel's cartilage.

• Journal of Oral Medicine and Pain
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• v.32 no.2
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• pp.137-150
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• 2007

Trees emit phytoncide into atmosphere to protect them from predation. Phytoncide from different trees has its own unique fragrance that is referred to as forest bath. Phytoncide, which is essential oil of trees, has microbicidal, insecticidal, acaricidal, and deodorizing effect. The present study was performed to examine the effect of phytoncide on Porphyromonas gingivalis, which is one of the most important causative agents of periodontitis and halitosis. P. gingivalis 2561 was incubated with or without phytoncide extracted from Hinoki (Chamaecyparis obtusa Sieb. et Zucc.; Japanese cypress) and then changes were observed in its cell viability, antibiotic sensitivity, morphology, and biochemical/molecular biological pattern. The results were as follows: 1. The phytoncide appeared to have a strong antibacterial effect on P. gingivalis. MIC of phytoncide for the bacterium was determined to be 0.008%. The antibacterial effect was attributed to bactericidal activity against P. gingivalis. It almost completely suppressed the bacterial cell viability (>99.9%) at the concentration of 0.01%, which is the MBC for the bacterium. 2. The phytoncide failed to enhance the bacterial susceptibility to ampicillin, cefotaxime, penicillin, and tetracycline but did increase the susceptibility to amoxicillin. 3. Numbers of electron dense granules, ghost cell, and vesicles increased with increasing concentration of the phytoncide, 4. RT-PCR analysis revealed that expression of superoxide dismutase was increased in the bacterium incubated with the phytoncide. 5. No distinct difference in protein profile between the bacterium incubated with or without the phytoncide was observed as determined by SDS-PAGE and immunoblot. Overall results suggest that the phytoncide is a strong antibacterial agent that has a bactericidal action against P. gingivalis. The phytoncide does not seem to affect much the profile of the major outer membrane proteins but interferes with antioxidant activity of the bacterium. Along with this, yet unknown mechanism may cause changes in cell morphology and eventually cell death.

• Journal of the Korean Society of Food Science and Nutrition
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• v.38 no.11
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• pp.1535-1542
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• 2009

To find the new use of Korean ginseng and mushroom, crude polysaccharides were prepared from submerged cultures of Hericium erinaceum in the medium supplemented with Korean ginseng extracts. When we fractionated crude polysaccharides (HE-GE-CP-1, 3, and 5) from hot-water extracts of submerged cultures of H. erinaceum with ginseng extracts (1%, 3%, and 5% addition of total medium), the yields of HE-GE-CP-1, 3, and 5 were identified at 5.7, 5.1, and 4.8%, respectively. Among crude polysaccharide fractions, HE-GE-CP-5 was significantly higher (1.89-fold of the saline control) than those of HE-GE-CP-1 (1.64-fold) or HE-GE-CP-3 (1.76-fold) on mitogenic activity of splenocytes. HE-GE-CP-5 also had the more potent bone marrow cell proliferation (1.83-fold) rather than HE-CP or HE-GE-CP-1 or HE-GE-CP-3 (1.59- or 1.44- or 1.69-fold, respectively), and anti-metastatic activity as anti-cancer effect showed the highest prophylactic value (72.4% inhibition of tumor control) in 5% supplementation of ginseng extract. However, the lysosomal phosphatase of macrophage was significantly stimulated after HE-GE-CP-3 treatment (2.03-fold). In addition, the immunostimulating and anti-metastatic crude polysaccharide, HE-GE-CP-5, contained mainly neutral sugars (63.2%) with considerable amounts of uronic acid (19.3%) and a small amount of proteins (8.8%). HE-GE-CP-5 can stimulate immune system to inhibit tumor metastasis, and its anti-tumor metastasis may be associated with macrophages, splenocytes and Peyer's patch cells activation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.8
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• pp.1158-1165
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• 2014

This study investigated the anti-inflammatory effects of Sargassum fulvellum ethanol extract (SFEE) on the lipopolysaccharide (LPS)-induced inflammatory response. SFEE remarkably suppressed production of NO and pro-inflammatory cytokines (IL-6, $TNF-{\alpha}$, and $IL-1{\beta}$ at 50 and $100{\mu}g/mL$. There were no cytotoxic effects on proliferation of macrophages treated with SFEE compared to the control. SFEE reduced expression of iNOS and COX-2 proteins in a dose-dependent manner. The formation of edema in mouse ears was reduced at the highest dose tested compared to the control. Moreover, in the acute toxicity test, no mortality occurred in mice administered 5,000 mg/kg body weight of SFEE over the 2-week observation period. These results suggest that SFEE may have significant effects on inflammatory factors and be a potential anti-inflammatory therapeutic material.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.4
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• pp.417-425
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• 2017

Cnidium monnieri (L.) Cusson is distributed in China and Korea, and the fruit of C. monnieri is used as traditional Chinese medicine to treat carbuncle and pain in female genitalia. In this study, we examined the anti-proliferation and cell cycle arrest effects of ethanol extracts from C. monnieri (CME) in AGS gastric cancer cells. Our results show that CME suppressed cell proliferation and induced release of lactate dehydrogenase (LDH) in AGS cells by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide assay and LDH assay. Cell morphology was altered by CME in a dose-dependent manner. In order to identify the cell cycle arrest effects of CME, we investigated cell cycle analysis after CME treatment. In our results, CME induced cell cycle arrest at G1 phase. Protein kinase B (Akt) plays a major role in cell survival mechanisms such as growth, division, and metastasis. Akt protein regulates various downstream proteins such as glycogen synthase kinase-$3{\beta}$ (GSK-$3{\beta}$) and tumor protein p53 (p53). Expression levels of p-Akt, p-GSK-$3{\beta}$, p53, p21, cyclin E, and cyclin-dependent kinase 2 (CDK2) were determined by Western blot analysis. Protein levels of p-Akt, p-GSK-$3{\beta}$, and cyclin E were reduced while those of p53, p21, and p-CDK2 (T14/Y15) were elevated by CME. Moreover, treatment with CME, LY294002 (phosphoinositide 3-kinase/Akt inhibitor), BIO (GSK-$3{\beta}$ inhibitor), and Pifithrin-${\alpha}$ (p53 inhibitor) showed that cell cycle arrest effects were mediated through regulation of the Akt/GSK-$3{\beta}$/p53 signaling pathway. These results suggest that CME induces cell cycle arrest at G1 phase via the Akt/GSK-$3{\beta}$/p53 signaling pathway in AGS gastric cancer cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.10
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• pp.1164-1170
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• 2017

Protaetia brevitarsis larvae (PBL) has recently been registered as a temporary food in Korea, and this study evaluated the application potential of PBL proteins as health functional food materials. Protein hydrolysates were prepared from PBL powder by enzymatic hydrolysis using five different proteases (alcalase, bromelain, flavourzyme, neutrase, and papain), and based on the results from the peptide content and SDS-PAGE analyses, PBL treated with alcalase or flavourzyme showed a high degree of hydrolysis (HD) value, whereas the HD value of those treated with neutrase, bromelain, or papain was minimal. The protein hydrolysates showing a high HD value were separated further into the fractions of >3 kDa and <3 kDa by a centrifugal filter system and then lyophilized, and according to the $RC_{50}$ values of the protein hydrolysates (<3 kDa) obtained from three different antioxidant analyses; the alcalase hydrolysates showed the highest antioxidant activity. Therefore, the alcalase hydrolysates were tested further for their inhibitory effects on the peroxidation of linoleic acid by measuring the thiobarbituric acid values. The results showed that the peroxidation of untreated linoleic acid increased dramatically during 6 days of incubation, but a pretreatment with the hydrolysates ($100{\sim}800{\mu}g/mL$) significantly inhibited the linoleic acid peroxidation in a dose-dependent manner for 6 days. Our current studies are focused on the identification of active peptide sequences from alcalase hydrolysates.

• Journal of the korean academy of Pediatric Dentistry
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• v.33 no.1
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• pp.13-24
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• 2006

Neuronal apoptotic events, consequently resulting in neuronal cell death, are occurred in hypoxic/ischemic condition. This cell death has been shown to be accompanied with the production of reactive oxygen species (ROS), which can attack cellular components such as nucleic acids, proteins and phospholipid. However, the underlying mechanisms of apoptosis induced in hypoxic/ischemic condition and its treatment methods are unsettled. Cobalt chloride $(CoCl_2)$ has been known to mimic hypoxic condition including the production of ROS. Epigallocatechin gallate (EGCG), a green tea polyphenol, has diverse pharmacologial activities in cell growth and death. This study was aimed to investigate the apoptotic mechanism by $CoCL_2$ and effects of EGCG on $CoCl_2-induced$ apoptosis in PC12 cells. Administration of $CoCl_2$ decreased cell survival in dose- and time-dependent manners and induced genomic DNA fragmentation. Treatment with $100{\mu}M$ EGCG for 30 min before PC12 cells were exposed to $150{\mu}M$ $CoCl_2$, being resulted in the cell viability and DNA fragmentation being rescued. $CoCl_2$ caused morphologic changes such as cell swelling and condensed nuclei whereas EGCG attenuated morphologic changes by $CoCl_2$. EGCG suppressed the apoptotic peak and a loss of ${\Delta}{\psi}_m$ induced by $CoCl_2$. $CoCl_2$ decreased Bcl-2 expression but Bax expression was not changed in $CoCl_2$- treated cells. EGCG attenuated the Bcl-2 underexpression by $CoCl_2$. $CoCl_2$ augumented the cytochrome c release from mitochondria into cytoplasm and increased caspase-8, -9 and caspase-3 activity a marker of the apoptotic executing stage. EGCG ameliorated the incruement in caspase-8, -9 and -3 activity, and cytochrome c release by $CoCl_2$ NAC (N-acetyl-cysteine), a scavenger of ROS, attenuated $CoCl_2-induced$ apoptosis in consistent with those of EGCG. These results suggest that $CoCl_2$ induces apoptotic cell death through both mitochondria- and death receptor-dependent pathway and EGCG has neuroprotective effects against $CoCl_2-induced$ apoptosis in PC12 cells.

• Tuberculosis and Respiratory Diseases
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• v.41 no.3
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• pp.248-261
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• 1994

Background: Lectins are proteins or glycoproteins of non-immune origin that recognize a specific sequence of sugar residues. The availability of a large number of lectins has provided the capacity to identify selectively glycoconjugates possessing distinctive chemical structure in diverse sites of highly specialized biological activity. The purpose of the present study was to investigate the lectin binding patterns of various components in human pulmonary tubercles. Method: Biopsy specimens of tuberculous lung were obtained from male adult patients who underwent a surgical resection for severe pulmonary tuberculosis. The specimens were processed and stained with 13 kinds of biotinylated lectins according to some modification of Hsu and Raine's methods. Results: 1) In the caseous necrotic lesions, BS $I-B_4$ showed negative reaction and BS I were also negative except some irregularly-shaped cells located in the marginal zone. All other lectins, however, showed a positive reaction with various binding patterns. 2) The epithelioid cells were broadly divided into three groups according to the reaction patterns in the cytoplasms and cell membranes. 3) WGA, ECL, PHA-L, PHA-E and LCA showed strong staining in the lymphocytes. 4) SBA showed a different binding patterns between the endothelial layers located in the region beyond the fibrous layers and those located within the fibrous layers. 5) PNA showed a positive reaction in the outer 1/3 to 1/2 of the fibrous layer, but showed no staining in the inner 1/2 to 2/3 of the fibrous layers. Conclusion: The present lectin histochemical study provided a useful information to assess the characterization and distribution of various glycoconjugates in each constituent of human pulmonary tubercles. The results demonstrate structural differences in the glycoconjugate composition of various components of the tubercles and reveal changes in glycosylation in the components during soft tubercle formation. This study provides a new data useful for the studies on the pathogenesis and pathology of human pulmonary tubercles.

• Tuberculosis and Respiratory Diseases
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• v.48 no.6
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• pp.909-921
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• 2000

Background : Defects in apoptotic signaling pathways play important role in tumor initiation, progression, metastasis and resistance to treatment. Several proteins which may promote tumorigenesis by inhibiting apoptosis were identified. The survivin protein is the member of inhibitor of apoptosis protein(IAPs) family which inhibits apoptosis. Unlike other IAPs, it is expressed in during the fetal period but not in adult differentiated tissues. Many reports have stated that survivin is selectively expressed in many cancer cell lines and cancer tissues. We performed immunohistochemical analysis for survivin expression in non-mall cell lung cancer to get evaluate its clinical implication. Methods : Twenty nine surgically resected lung cancers were examined. Immunohistochemical staining were performed by immuno-peroxidase technique using avidin-biotinylated horseradish pemxidase complex in the formalin-fixed, paraffin-embedded tissue $4{\mu}m$ section. Anti-survivin polyclonal antibody was used for primary antibody and anti-p53 monoclonal antibody was also used to analyze the correlation between survivin and p53 expression. The survivin expression scores were determined by as the sum of the stained area and intensity. Results : Immunohistochemical analysis showed cancer specific expression of survivin in 20 of 29 cases (69.0%). Western blot analysis also showed the selective survivin expression in tumor tissue. There was no correlation between survivin expression and clinicopathological parameters and prognosis. We analyzed the ∞π'elation between survivin expression and p53 expression, but found none. Conclusion: We confirmed the tumor specific expression of survival in non-small cell lung canær. But this expression was not correlated with clinical parameters as well as histology, tumor stage, recurrence, and survival rate. Also it was not statistically correlated with the expression of p53.

• KSBB Journal
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• v.24 no.4
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• pp.403-409
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• 2009

H2AX, a crucial component of chromatin, is implicated in DNA repair, cell cycle check point and tumor suppression. The aim of this study was to identify direct binding partners of H2AX to regulate cellular responses to above mechanisms. Literature reviews and bioinformatical tools were attempted intensively to find binding partners of H2AX, which resulted in identifying two potential proteins, breast cancer-1 (BRCA1) and BRCA1-associated RING domain 1 (BARD1). Although it has been reported in vivo that BRCA1 co-localizes with H2AX at the site of DNA damage, their biochemical mechanism for H2AX were however only known that the complex monoubiquitinates histone monomers, including unphosphorylated H2AX in vitro. Therefore, it is important to know whether the complex directly interacts with H2AX, and also which regions of these are specifically mediated for the interaction. Using in vitro GST pull-down assay, we present here that BRCA1 and BARD1 directly bind to H2AX. Moreover, through combinational approaches of domain analysis, fragment clonings and in vitro binding assay, we revealed molecular details of the BRCA1-H2AX and BARD1-H2AX complex. These data provide the potential evidence that each of the BRCA1 nuclear localization signal (NLS) and BARD1 BRCA1 C-terminal (BRCT) repeat domain is the novel mediator of H2AX recognition.