• Maxillofacial Plastic and Reconstructive Surgery
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• v.21 no.3
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• pp.257-265
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• 1999

To investigate the sequential changes in microvascular architecture and osseous regeneration during the bony healing after an application of the guided tissue regeneration method, we made artificial defects measuring $0.7cm{\times}0.3cm$ in size on femoral bones of rats measuring about 200gm and applied non-absorbable TEFE membrane at experimental sites but not at control sites. Then we observed the sequential changes and correlations between new vacuolation and bony regeneration using microvascular corrosion cast method and routine light microscopic observation at 1, 2 and 3 weeks after operation, respectively. The results showed that there were close relationships between regeneration of microvasculature and bone. In early phase, the invasion of granulation tissue at control sites delayed bony regeneration, however, in later phase, there was no remarkable differences in bony regeneration between control and experimental sites. The placement of barrier also affected in revascularization of regenerating bony defects. This is, the experimental sites showed parallel arranged nutritional vessels along long axis with well developed retiform plexus whereas the control revealed vertical invasion of microvasculature from outside of marrow space through bony defects which was also rearrange with time into parallel pattern with a vertical plexus but lesser organized than that of experimental sites. These findings suggest that the reconstruction of regenerating vasculature within the marrow cavity only may be sufficient and/or more be efficient in regeneration of bony defects.

• Journal of Veterinary Clinics
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• v.30 no.1
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• pp.41-44
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• 2013

A 4-year-old castrated male Shih-Tzu was presented to the Chonbuk National University Animal Medical Center with a history of melting ulcer in the right eye (OD). Upon ophthalmologic examination, severe keratomalacia of approximately 70% of the entire surface area with a full thickness corneal defect was found in OD. In addition, iris and fibrin clots were observed on the center of the corneal defect. The menace response and dazzle reflex were normal in OS. As the size and damage of corneal perforation was so severe, amniotic membrane (AM) transplantation was considered to repair the cornea instead of direct suture technique, flap methods or corneal transplantation. Equine AM was sutured to the limbus to cover the entire cornea in a single interrupted pattern using 9-0 nylon suture material. On day 79, mild scarring and pigmentation, with almost no vasculature, remained. The menace response and dazzle reflex were normal of OD. Although pigmentation and scarring remained on the cornea, equine AM transplantation can be useful for reconstruction of severe corneal perforation with keratomalacia.

• Journal of Life Science
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• v.21 no.5
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• pp.664-670
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• 2011

Oxidative stress results in sustained release of heat shock protein 90 (HSP90) from vascular smooth muscle cells (VSMCs). We investigated whether extracellular HSP90 predisposed VSMCs to pro-inflammatory phenotype. Exposure of human aortic smooth muscle cells to HSP90 not only significantly enhanced CXCL10 secretion but also increased CXCL10 transcription. HSP90-mediated CXCL10 secretion was attenuated by OxPAPC, a TLR-2/4 inhibitor, and curcumin, a TLR-4 dimerization inhibitor. Inhibitors of diphenyleneiodium chloride and the Akt pathway also attenuated CXCL10 secretion in response to HSP90. The gene delivery of I${\kappa}$B using recombinant adenoviruses and treatment with resveratrol, which inhibit NF-${\kappa}$B activity, significantly attenuated HSP90-induced CXCL10 secretion from VSMCs. We propose that extracellular HSP90 contributes to an inflammatory reaction in the stressed vasculature by inducing CXCL10 expression of VSMCs, and that TLR-4, Akt, and NF-${\kappa}$B play active roles in the process.

• Korean Journal of Food Science and Technology
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• v.43 no.2
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• pp.206-212
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• 2011

Makgeolli is Korean traditional alcoholic beverage that has historically been brewed. In this study, we analyzed the profile of organic acids in makgeolli and also evaluated its physiological characteristics. Makgeolli contained excess lactic acid, which is produced by lactic acid bacteria (LAB). Anti-obesity effects of makgeolli were investigated in 3T3-L1 preadipocytes. Compared to the negative control, makgeolli inhibited the differentiation of preadipocyte as quantified by Oil red O dye. In particular, $100{\mu}g/mL$ makgeolli reduced 40 to 70% of differentiation. To evaluate the anti-angiogenic and anti-inflammatory effects of makgeolli, we performed chorioallantoic membrane assay and measured nitric oxide production from lipopolysaccharide-induced RAW264.7 cells. Most makgeolli interrupted the formation of neo-vasculature and significantly inhibited NO production in a dose-dependent manner. Taken together, these findings suggest that commercial makgeolli has inhibitory activities against adipogenesis, neo-vascularization, and inflammation, and also they are influenced by second metabolites from nuruk microflora containing fungi and LAB.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.59-67
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• 1982

1) Oxymetazoline, which has been known as an agonist for${\alpha}_1-adrenoceptor$ in various peripheral tissues, caused a pressor response in urethane-anesthetized rabbits when given intra-ventricularly. This pressor response was little affected by pretreatment of rabbits with i.v. guanethidine or chlorisondamine, but it was weakened in rabbits pretreated with either of i.v. phentolamine or guanethidine and chlorisondamine and in guanethidine-pretreated adrenal-ligated rabbits. 2) The pressor to intraventricular oxymetazoline was markedly attenuated by intraventricular pretreatment with prazosin, whereas intraventricular pretreatment with yohimbine or piperoxan did not affect this response. 3) Reserpine-pretreated rabbits also responded with hypertension to intraventricular oxymetazoline, which was markedly diminished by pretreatment with intraventricular prazosin but not affected by yohimbine. 4) Oxymetazoline, given intravenously, produced a pressor response in both whole and spinal rabbits. Intravenous prazosin, phentolamine and yohimbine, in this order, showed greater antagonizing effect to this pressor response. 5) The results indicate that oxymetazoline acts an agonist for ${\alpha}_1-adrenoceptors$ in the rabbit brain participating in the regulation of the blood pressure and in the vasculature of rabbits.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.2
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• pp.627-633
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• 2015

Background: To study the effect of parecoxib, a novel cyclooxygenase-2 selective inhibitor, on the radiation response of colorectal cancer (CRC) cells and its underlying mechanisms. Materials and Methods: Both in vitro colony formation and apoptosis assays as well as in vivo mouse xenograft experiments were used to explore the radiosensitizing effects of parecoxib in human HCT116 and HT29 CRC cells. Results: Parecoxib sensitized CRC cells to radiation in vitro with a sensitivity enhancement ratio of 1.32 for HCT116 cells and 1.15 for HT29 cells at a surviving fraction of 0.37. This effect was partially attributable to enhanced apoptosis induction by parecoxib combined with radiation, as illustrated using an in vitro apoptosis assays. Parecoxib augmented the tumor response of HCT116 xenografts to radiation, achieving growth delay more than 20 days and an enhancement factor of 1.53. In accordance with the in vitro results, parecoxib combined with radiation resulted in less proliferation and more apoptosis in tumors than radiation alone. Radiation monotherapy decreased microvessel density (MVD) and microvessel intensity (MVI), but increased the hypoxia level in xenografts. Parecoxib did not affect MVD, but it increased MVI and attenuated hypoxia. Conclusions: Parecoxib can effectively enhance radiation sensitivity in CRC cells through direct effects on tumor cells and indirect effects on tumor vasculature.

• Journal of Life Science
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• v.20 no.2
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• pp.169-175
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• 2010

Intestinally absorptive and distributive aspects of the subtoxic level of selenite in rats were investigated using a double perfusion system. The double-perfusion technique is an in situ, in vitro preparation in which the intestinal lumen and its vasculature are perfused simultaneously. In the previous study, the subtoxic level of sodium selenite was determined to be 1.2 mM through inhibition of 3-0-methyl glucose (3MG) absorption. Thus, the selenite used to identify the intestinally absorptive mechanism of selenite was perfused at a luminal concentration of 1, 10, 50, 100 and $200\;{\mu}M$. Appearance of radiolabeled-Selenium (Se) was identified in three compartments: luminal perfusate, small intestine and vascular perfusate. Dose-response curves for Se in the three compartments indicate that selenite is absorbed by non-mediated passive diffusion. Regarding the distributive aspect, $21.02{\pm}3.92%$ of the total amount of selenite in the lumen was transported into the blood vessels across the small intestine. However, $4.75{\pm}1.75%$ of the total amount of selenite in the lumen is retained by the small intestine. Therefore, a total of $25.67{\pm}4.46%$ of the test dose was taken up from the luminal perfusate.

• Journal of Life Science
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• v.18 no.11
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• pp.1513-1520
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• 2008

The 4-Hydroxynonenal (HNE) affects vascular dysfunctions probably through the interruption of the cellular redox balance. To better understand vascular abnormalities resulting from the accumulation of HNE, we delineated mechanism by which mitochondrial apoptosis occurs in the YPEN-1 endothelial cells. HNE treatment led to the loss of mitochondrial membrane potential (${\delta}{\Psi}_m$), resulting in the release of cytochrome c. Data showed decreased Bcl-2 and increased Bax protein levels in HNE-treated cells. NAC, a reactive oxygen species (ROS) scavenger, and penicillamine, the peroxynitrite scavenger, blocked HNE-mediated ROS generation, thereby thwarting the cytochrome c release and apoptosis. The treatment of the cells with zVAD-fmk, a broad range caspase inhibitor did not suppress HNE-induced apoptosis, suggesting that the apoptosis might be the possibility of caspase-independent process. Our findings delineate the underlying mechanism of the HNE induced endothelial apoptosis by triggering depolarization of mitochondria membrane potential that can lead to the deterioration of vasculature homeostasis and subsequent vascular dysfunction with aging.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.4
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• pp.1589-1595
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• 2014

Objective: Forkhead box C2 (FOXC2) is a member of the winged helix/forkhead box (Fox) family of transcription factors. It has been suggested to regulate tumor vasculature, growth, invasion and metastasis, although it has not been studied in cervical cancer. Here, we analyzed FOXC2 expression in cervical tissues corresponding to different stages of cervical cancer development and examined its correlation with clinicopathological characteristics. In addition, we examined the effects of targeting FOXC2 on the biological behavior of human cervical cancer cells. Methods: The expression of FOXC2 in normal human cervix, CIN I-III and cervical cancer was examined by immunohistochemistry and compared among the three groups and between cervical cancers with different pathological subtypes. Endogenous expression of FOXC2 was transiently knocked down in human Hela and SiHa cervical cells by siRNA, and cell viability and migration were examined by scratch and CCK8 assays, respectively. Results: In normal cervical tissue the frequency of positive staining was 25% (10/40 cases), with a staining intensity (PI) of $0.297{\pm}0.520$, in CIN was 65% (26/40cases), with a PI of $3.00{\pm}3.29$, and in cancer was 91.8% (68/74 cases), with a PI of $5.568 {\pm}3.449$. The frequency was 100% in adenocarcinoma (5/5 cases) and 91.3% in SCCs (63/69 cases). The FOXC2 positive expression rate was 88.5% in patients with cervical SCC stage I and 100% in stage II, showing significant differences compared with normal cervix and CIN. With age, pathologic differentiation degree and tumor size, FOXC2 expression showed no significant variation. On transient transfection of Hela and SiHa cells, FOXC2-siRNA inhibition rates were 76.2% and 75.7%; CCK8 results showed reduced proliferation and relative migration (in Hela cells from $64.5{\pm}3.16$ to $49.5{\pm}9.24$ and in SiHa cells from $60.1{\pm}3.05$ to $44.3{\pm}3.98$) (P < 0.05). Conclusion: FOXC2 gene expression increases with malignancy, especially with blood vessel hyperplasia and invasion degree. Targeted silencing was associated with reduced cell proliferation as well as invasion potential.

• Proceedings of the Korean Society of Crop Science Conference
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• 2017.06a
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• pp.159-159
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• 2017

Drought, a common environmental constraint, induces a range of physiological, biochemical and molecular changes in plants, and can cause severe reductions in crop yield. Consequently, understanding the molecular mechanisms of drought tolerance is an important step towards crop biotechnology. Here, we report that the rice (Oryza sativa) homeodomain-leucine zipper class IV transcription factor gene, ${\underline{R}ice}$ ${\underline{o}utermost}$ ${\underline{c}ell-specific}$ gene 10 (Roc10), enhances drought tolerance and grain yield by increasing lignin accumulation in ground tissues. Overexpression of Roc10 in rice significantly increased drought tolerance at the vegetative stages of growth and promoted both more effective photosynthesis and a reduction in water loss rate, compared with non-transgenic controls or RNAi transgenic plants. Importantly, Roc10 overexpressing plants had a higher drought tolerance at the reproductive stage of growth and a higher grain yield compared with the controls under field-drought conditions. Roc10 is mainly expressed in outer cell layers including the epidermis and the vasculature of the shoots, which coincides with areas of cell wall lignification. Roc10 overexpression elevated the expression levels of lignin biosynthetic genes in shoots, with a concomitant increase in the accumulation of lignin, while the overexpression and RNAi lines showed opposite patterns of lignin accumulation. We identified downstream target genes of Roc10 by performing RNA-seq and chromatin immunoprecipitation (ChIP)-seq analyses of shoot tissues. Roc10 was found to directly bind to the promoter of PEROXIDASEN/PEROXIDASE38, a key gene in lignin biosynthesis. Together, our findings suggest that Roc10 confers drought stress tolerance by promoting lignin biosynthesis in ground tissues.