• Molecules and Cells
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• v.24 no.1
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• pp.69-75
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• 2007

Alzheimer's disease is a neurodegenerative disorder associated with progressive loss of cognitive function and memory. Amyloid beta peptide ($A{\beta}$) is the major component of senile plaques and is known to exert its cytotoxic effect mainly by producing $H_2O_2$. Vascular endothelial growth factor (VEGF) is elevated in the cerebrospinal fluid (CSF) and brain of AD patients, and $H_2O_2$ is one of the factors that induce VEGF. Therefore, we tested whether $A{\beta}$ might be responsible for the increased VEGF synthesis. We found that $A{\beta}$ induced the production of $H_2O_2$ in vitro. Comparison of the amount of $H_2O_2$ required to induce VEGF synthesis in HN33 cells and the amount of $H_2O_2$ produced by $10{\mu}M\;A{\beta}_{1-42}$ in vitro suggested that a toxic concentration of $A{\beta}$ might induce VEGF synthesis in these cells. However, toxic concentrations of $A{\beta}$ failed to induce VEGF synthesis in several cell systems. They also had no effect on antioxidant enzymes such as glutathione peroxidase, catalase, and peroxiredoxin in HN33 cells. $Cu^{2+}$, $Zn^{2+}$ and $Fe^{3+}$ are known to accumulate in the brains of AD patients and promote aggregation of $A{\beta}$, and $Cu^{2+}$ by itself induces synthesis of VEGF. However, there was no synergistic effect between $Cu^{2+}$ and $A{\beta}_{1-42}$ in the induction of VEGF synthesis and $Zn^{2+}$ and $Fe^{3+}$ also had no effect on the synthesis of VEGF, alone or in combination with $A{\beta}$.

• Archives of Plastic Surgery
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• v.44 no.2
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• pp.95-100
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• 2017

Background Intima-to-intima microanastomotic vascular remodeling was explored, utilizing a polylactide-caprolactone absorbable vein coupler model (PAVCM), which was designed to simulate a non-absorbable counterpart system with the sole exception of being absorbable. Methods Six New Zealand white rabbits were used. After transection of the jugular vein, 2 PAVCMs were placed, 1 at each transected end. The stumps were slipped through the PAVCMs, and the venous wall was everted $90^{\circ}$ to achieve intima-to-intima contact. Reanastomosis of the transected jugular vein was performed bilaterally in 3 rabbits. In the other 3 rabbits, the jugular vein (20 mm) harvested from one side was interpositionally grafted to the jugular vein on the opposite side to ease the anastomotic tension. Patency testing, ultrasonography, and histologic assessments were conducted postoperatively at weeks 2, 4, 12, 16, 22, and 26. Results All anastomotic sites were patent, without stenosis, occlusion, or dilatation. In the histologic sections, immature endothelial regeneration was observed at week 2, which was completed by week 4. Regeneration of the tunica media was noted at week 12. Between week 22 and week 26, the tunica media fully regenerated and the coupler dissipated entirely. Conclusions Despite the absence of a coupler to act as an anastomotic buttress, the structure and function of all the vessels appeared normal, even histologically. These outcomes are true milestones in the development of an absorbable vein coupler.

• Proceedings of the Ginseng society Conference
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• 1993.09a
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• pp.40-48
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• 1993

Intravenous administration of saponin extracted from the root of Panax ginseng lowered the blood pressure dose-dependently (10-200 mg/kg, B.W) in anesthetized rats. Therefore, experiments were designed to study the hypothesis that the lowering of blood pressure is associated with the release of endothelium-derived relaxing factor and the accumulation of guanosine 3, 5-cyclic monophosphate (cGMP). Rings of thoracic aorta with and without endothelium were suspended for the measurement of isometric tension in organ chamber and the tissue content of cGMP was measured by radioimmunoassay. All experiments were performed in the presence of $indomethacin(10^{-5}M).$ Ginseng saponin $(10^{-5}-3{\times}10^{-6}g/ml)$ relaxed contractions induced by phenylephrine $10^{-6}M)$ in the aorta with endothelium but not in that without endothelium. Treatment of aortic rings with $N^G$ monomethyl-L-arginine (L-NMMA, $10^{-4}M$ for 30 min), a competitive inhibitor of nitric oxide synthase, and methylene blue $(MB,\;3{\times}10^{-7}M$ for 30 min). an inhibitor of soluble guanylate cyclase, diminished the relaxation induced by Ginseng saponin. Ginseng saponin $10^{-4}g/ml$ for 2 min) increased the accumulation of cGMP in rings with endothelium. L-NMMA and MB inhibited the accumulation of cGMP induced by Ginseng saponin. These data suggest that vascular relaxations induced by Ginseng saponin are mediated by release of endothelium-derived relaxing factor and the accumulation of cGMP. The effect of Ginseng saponin on endothelial function in hypercholesterolemic rabbits was examined. In hypercholesterolemic rabbits fed with $2\%$ cholesterol for 8 weeks, relaxation of aortic rings to acetylcholine was impaired. The impaired relaxations of aortic rings in hypercholesterolemic rabbits were improved by dietary supplementation of Ginseng saponin, probably because of an improved release of endothelium - derived relaxing factor.

• Current Optics and Photonics
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• v.3 no.6
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• pp.485-495
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• 2019

Photobiomodulation (PBM) using organic light emitting diodes (OLEDs) surface light sources have recently been claimed to be the next generation of PBM light sources. However, the differences between light emitting diodes (LEDs) and OLED mechanisms in vitro and in vivo have not been well studied. In vivo mouse models were used to investigate the effects of OLED irradiation on cellular function and cutaneous wound healing compared to LED irradiation. Mice in the LED- and OLED-irradiated groups were subjected to irradiation with 6 J/㎠ LED and OLED (630 nm), respectively, for 14 days after wounding, and some mice were sacrificed for the experiments on days 3, 7, 10, and 14. To evaluate wound healing, we performed hematoxylin-eosin and Masson's trichrome staining and quantified collagen density by computerized image analysis. The results showed that the size of the wound, collagen density, neo-epidermis thickness, number of new blood vessels, and number of fibroblasts and neutrophils was significantly influenced by LED and OLED irradiation. The tissue levels of interleukin (IL)-β, IL-6 and tumor necrosis factor (TNF)-α were investigated by immunohistochemical staining. LED and OLED irradiation resulted in a significant increase in the tissue IL-β and IL-6 levels at the early stage of wound healing (P < 0.01), and a decrease in the tissue TNF-α level at all stages of wound healing (P < 0.05), compared to the no-treatment group. The expression levels of the genes encoding vascular endothelial growth factor and transforming growth factor-beta 1 were significantly increased in LED and OLED-irradiated wound tissue at the early stage of wound healing (P < 0.01) compared to the no-treatment group. Thus, OLED as well as LED irradiation accelerated wound healing by modulating the synthesis of anti-inflammatory cytokines and the expression levels of genes encoding growth factors, promoting collagen regeneration and reducing scarring. In conclusion, this suggests the possibility of OLED as a new light source to overcome the limitations of existing PBMs.

• Journal of the korean academy of Pediatric Dentistry
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• v.36 no.4
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• pp.586-590
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• 2009

Leukocyte adhesion deficiency is rare inherited defect on phagocytic function resulting lack of leukocyte cell surface expression of $\beta2$ integrin molecule that are essential for leukocyte adhesion to endothelial cells and chemotaxis. Clinical features of patients with leukocyte adhesion deficiency type I include recurrent necrotic infection of the skin mucous membranes, and intestinal tract with septicemia, and omphalitis arising from delayed umbilical cord separation. Oral manifestations are severe progressive periodontitis with alveolar bone loss, periodontal pockets, and partial and total premature loss of the deciduous and permanent dentitions. We report a case of leukocyte adhesion deficiency type I in a 5-year-old child with severe periodontitis. In order to prevent local and systemic infection, we controlled periodontal disease with periodic oral prophylaxis. Oral swabs and blood cultures were perfomed for suspected infection, so that optimal measures were taken through the use of appropriate antibiotics.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.10
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• pp.5579-5587
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• 2013

Research indicates that a small population of cancer cells is highly tumorigenic, endowed with the capacity for self-renewal, and has the ability to differentiate into cells that constitute the bulk of tumors. These cells are considered the "drivers" of the tumorigenic process in some tumor types, and have been named cancer stem cells (CSC). Epithelial-mesenchymal transition (EMT) appears to be involved in the process leading to the acquisition of stemness by epithelial tumor cells. Through this process, cells acquire an invasive phenotype that may contribute to tumor recurrence and metastasis. CSC have been identified in human head and neck squamous cell carcinomas (HNSCC) using markers such as CD133 and CD44 expression, and aldehyde dehydrogenase (ALDH) activity. Head and neck cancer stem cells reside primarily in perivascular niches in the invasive fronts where endothelial-cell initiated events contribute to their survival and function. Clinically, CSC enrichment has been shown to be enhanced in recurrent disease, treatment failure and metastasis. CSC represent a novel target of study given their slow growth and innate mechanisms conferring treatment resistance. Further understanding of their unique phenotype may reveal potential molecular targets to improve therapeutic and survival outcomes in patients with HNSCC. Here, we discuss the state-of-the-knowledge on the pathobiology of cancer stem cells, with a focus on the impact of these cells on head and neck tumor progression, metastasis and recurrence due to treatment failure.

• Journal of Korean Neurosurgical Society
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• v.63 no.4
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• pp.444-454
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• 2020

Objective : Glioblastoma multiforme (GBM) is the most aggressive for of brain tumor and treatment often fails due to the invasion of tumor cells into neighboring healthy brain tissues. Activation of the Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway is essential for normal cellular function including angiogenesis, and has been proposed to have a pivotal role in glioma invasion. This study aimed to determine the dose-dependent effects of ruxolitinib, an inhibitor of JAK, on the interferon (IFN)-I/IFN-α/IFN-β receptor/STAT and IFN-γ/IFN-γ receptor/STAT1 axes of the IFN-receptor-dependent JAK/STAT signaling pathway in glioblastoma invasion and tumorigenesis in U87 glioblastoma tumor spheroids. Methods : We administered three different doses of ruxolitinib (50, 100, and 200 nM) to human U87 glioblastoma spheroids and analyzed the gene expression profiles of IFNs receptors from the JAK/STAT pathway. To evaluate activation of this pathway, we quantified the phosphorylation of JAK and STAT proteins using Western blotting. Results : Quantitative real-time polymerase chain reaction analysis demonstrated that ruxolitinib led to upregulated of the IFN-α and IFN-γ while no change on the hypoxia-inducible factor-1α and vascular endothelial growth factor expression levels. Additionally, we showed that ruxolitinib inhibited phosphorylation of JAK/STAT proteins. The inhibition of IFNs dependent JAK/STAT signaling by ruxolitinib leads to decreases of the U87 cells invasiveness and tumorigenesis. We demonstrate that ruxolitinib may inhibit glioma invasion and tumorigenesis through inhibition of the IFN-induced JAK/STAT signaling pathway. Conclusion : Collectively, our results revealed that ruxolitinib may have therapeutic potential in glioblastomas, possibly by JAK/STAT signaling triggered by IFN-α and IFN-γ.

• Development and Reproduction
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• v.19 no.4
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• pp.227-234
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• 2015

The objective of this study was to investigate the expression of bovine luteum expressed sequence tags (ESTs), vascular endothelial growth factor (VEGF), and tumor necrosis factor receptor 1 (TNFR1) and the presence of functional ESTs in the bovine corpus luteum (CL) during different stages of the estrus cycle. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed a difference in the expression of ESTs during the CL stage. Concentration of ESTs in the CL tissue increased significantly from the mid-luteal stage and decreased thereafter. RT-PCR analysis showed higher levels of the EST genes in the CL of the mid-luteal stage than in other stages, and the same level of expression of VEGF. Immunohistochemistry analysis of the tissue from CL formation to regression showed low cytosol and aggregation of the nucleus. And activity caspase 3 (apoptosis detector) was most strongly detected in the CL1 stage of bovine. During the estrous cycle, the cytosol was magnified and differentiation of the nucleus was clearly manifested. The ESTs affected the CL, and the relationship between VEGF and TNFR1 played a pivotal role for CL development and activation, dependent on the stage of CL. These results suggest local production of ESTs, the presence of functional ESTs in the bovine CL, and that ESTs play a role in regulating the function of cell death in bovine CL.

• The Korean Journal of Food And Nutrition
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• v.31 no.3
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• pp.328-334
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• 2018

The purpose of this study was to examine the effects of Maca water and/or ethanol extract on the nitric oxide (NO) production in human umbilical vein endothelial cells HUVAC and on erectile dysfunction in rats. Maca was extracted due to both solutions, which are water and ethanol. Each Maca extract was applied to HUVAC, and NO production was checked. Additionally, three different dosages (250, 500 and 1,000 mg/kg) of Maca ethanol extract was administered to Sprague-Dawley rats for 4 weeks. All rats were sacrificed and each sample was collected for analysis. The control rats received only the saline vehicle. The NO production of HUVAC was significantly increased by domestic and homemade Maca water extracted at $60^{\circ}C$ group. Both NO generation and testosterone release were not influenced due to the oral administration of Maca. In the EtOH group rats, the number of sperm was reduced compared to that of the control group. All Maca groups had a high number of sperm and each sperm count had increased as a result of the Maca extract dose. The results of this research suggest that Maca has a positive effect on male erectile dysfunction, which need to be examined further in future studies.

• Journal of Veterinary Clinics
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• v.22 no.3
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• pp.220-227
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• 2005

Although ketamine has been used in the field of anesthetic medicine for its safety and favourable respiratory effects, the cardiovascular effects of ketamine is still controversial. To clarify the action and mechanism of ketamine upon cardiovascular system, arterial blood pressure, tension of aortic ring, left ventricular developed pressure and heart rate were measured in rats, Ketamine produced two types of effects on arterial blood pressure in anesthetized rats; monophasic effect (blood pressure lowering) and biphasic effect (initial transient blood pressure increasing following sustained lowering), The ketamine-induced lowering of aterial blood pressure showed a concentration-dependent manner, inhibited by the pretreament of $MgCl_2$ and potentiated by the pretreatment of $CaCl_2$. The ketamine-induced lowering of aterial blood pressure was suppressed by the pretreatment of nifedipine, verapamil or lidocaine. In phenylephrine-precontracted endothelium intact (+E) aortic rings, ketamine sometimes caused a small enhancement of contraction ($112.5{\pm}3.6{\%}$). However, in many experiments, ketamine produced a concentration-dependent relaxation in +E aortic rings precontracted with either phenylephrine or KCl. Ketamine-induced relaxation was significantly greater in KCl-precontracted strips than phenylephrine-precontracted strips. In phenylephrine-precontracted +E aortic rings, the ketamine-induced vasorelaxation was not suppressed by endothelium removal or by the pretreatment of a nitric oxide synthase inhibitors, L-$N^G$-nitro-arginine and a guanylate cyclase inhibitors, methylene blue, suggesting that the ketamine-induced vasorelaxation is not dependent on the endothelial function. In addition, ketamine elicited an increase in left ventricular developed pressure in perfused hearts accompanied by decrease in heart rate. These results suggest that ketamine could evoke a hypotension due to vasorelaxation and decrease in heart rate in rats. The inhibitory effect of cardiovascular system might be associated with modulation of $Ca^{2+}$ homeostasis.