Daejeon, South Korea
Daejeon, South Korea

Chungnam National University is one of ten Flagship Korean National Universities. It is recognized as one of the most prestigious five national universities in Korea. Wikipedia.


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Patent
Chungnam National University | Date: 2016-09-22

The present invention relates to a transfer-free method for forming a graphene layer, in which a high-quality graphene layer having excellent crystallinity can be easily formed over a large area at low temperature by a transfer-free process so that it can be applied directly to a base substrate, which is used in a transparent electrode, a semiconductor device or the like, without requiring a separate transfer process, and to an electrical device comprising a graphene layer formed by the method. More specifically, the transfer-free method for forming a graphene layer comprises the steps of: depositing a Ti layer having a thickness of 3-20 m on a base substrate by sputtering; and growing graphene on the deposited Ti layer by chemical vapor deposition.


Patent
Chungnam National University | Date: 2016-12-09

A method for cell-free protein synthesis is characterized in that pH is controlled by using an enzyme. For example, by using an amino acid decarboxylase, the pH is controlled according to removal of hydrogen ions that are produced during regeneration of ATP. The method for cell-free protein synthesis of the present invention has an advantage that not only the expression amount of protein is enhanced but also the expressed protein can be directly used for activity analysis without undergoing any separation or purification.


Patent
Samsung, Chungnam National University and Korea Research Institute of Chemical Technology | Date: 2016-09-23

An electrically conductive composite including: a polymer matrix including a cellulose, and a plurality of electrically conductive carbon nanoparticles dispersed in the polymer matrix, wherein the electrically conductive carbon nanoparticles have a multiple hydrogen bonding moiety covalently bound to a surface thereof.


Disclosed is a new compound that inhibits binding between a DX2 protein and a p14/ARF protein, a pharmaceutical composition including the new compound as an effective component for treating or preventing a cancer disease, an anticancer adjuvant for improving an anticancer effect of a drug-resistant anticancer drug, and a composition including an AIMP2-DX2 protein or a fragment thereof for diagnosing lung cancer.


The present invention relates to a new compound for inhibiting binding between a DX2 protein and a p14/ARF protein, and a medical use thereof. A review of the in vitro and in vivo anticancer effect of the compound shows that the compound has an excellent anticancer effect and thus is useful as a drug for treating various cancer diseases including lung cancer, and has a more improved anticancer effect particularly by inhibiting resistance to an anticancer drug of Adriamycin in a cell line which is resistant to an anticancer drug such as Adriamycin, and thus can be used as an anticancer adjuvant for improving the anticancer effect. In addition, the present invention relates to a composition for diagnosing lung cancer comprising an AIMP2-DX2 protein or a fragment thereof, and is effective in diagnosis of lung cancer because whether or not a subject has lung cancer is confirmed only by using a serum sample of the subject.


News Article | May 18, 2017
Site: www.sciencedaily.com

A team led by KOH Gou Young, director of the Center for Vascular Research, within the Institute for Basic Science (IBS), in collaboration with Chungnam National University, clarified the molecular mechanism to explain how the thyroid and surrounding vascular system change in the most common form of hyperthyroidism. Published in the EMBO Molecular Medicine journal, these findings provide a potential therapeutic target for thyroid diseases. The thyroid is a highly vascularized organ, found behind the Adam's apple. Some of the functions of the thyroid are regulated by a hormone, called thyrotropin, produced in the brain. Graves' disease, the most common cause of hyperthyroidism in the United States, affects both the thyroid and the surrounding vascular network. In this disease, the thyroid produces an excessive amount of hormones and the capillaries become denser. "Previous studies show that abnormalities in thyroid glands and surrounding vasculature are interconnected, we wanted to understand how this happens, at the molecular level," explains Koh. Using animal models that simulate Graves' disease, IBS scientists uncovered the biological pathway contributing to this disorder. They found that the culprit is the vascular endothelial growth factor A (VEGF-A). This protein is involved in forming new vessels around the thyroid, and regulating the hormonal exchange happening between these vessels and the thyroid, through very small pores called fenestrae (from Latin 'window'). Upon stimulation with the thyrotropin hormone, VEGF-A is produced by the thyroid gland and as a result, the thyroid enlarges and the walls of the capillaries (constituted mainly by endothelial cells) increase the expression of VEGFR2, the receptor for VEGF-A. By blocking VEGFR2, IBS scientists could inhibit enlargement of the thyroid and stop vascular remodeling. "Our findings identify VEGFR2 blockade as a novel therapeutic avenue for targeting thyroid disease associated with thyrotropin," explains Koh. Concurrently, the research team could also exclude other molecular pathways. For example, they found that the angiopoietin-Tie2 pathway, fundamental in other tissues like the eyes and brain, does not play a major role in remodeling the vasculature of the thyroid gland. Finally, VEGFR3 was ruled out from the indispensable pool of proteins that maintain thyroid vascular integrity.


News Article | May 18, 2017
Site: www.eurekalert.org

A team led by KOH Gou Young, director of the Center for Vascular Research, within the Institute for Basic Science (IBS), in collaboration with Chungnam National University, clarified the molecular mechanism to explain how the thyroid and surrounding vascular system change in the most common form of hyperthyroidism. Published in the EMBO Molecular Medicine journal, these findings provide a potential therapeutic target for thyroid diseases. The thyroid is a highly vascularized organ, found behind the Adam's apple. Some of the functions of the thyroid are regulated by a hormone, called thyrotropin, produced in the brain. Graves' disease, the most common cause of hyperthyroidism in the United States, affects both the thyroid and the surrounding vascular network. In this disease, the thyroid produces an excessive amount of hormones and the capillaries become denser. "Previous studies show that abnormalities in thyroid glands and surrounding vasculature are interconnected, we wanted to understand how this happens, at the molecular level," explains Koh. Using animal models that simulate Graves' disease, IBS scientists uncovered the biological pathway contributing to this disorder. They found that the culprit is the vascular endothelial growth factor A (VEGF-A). This protein is involved in forming new vessels around the thyroid, and regulating the hormonal exchange happening between these vessels and the thyroid, through very small pores called fenestrae (from Latin 'window'). Upon stimulation with the thyrotropin hormone, VEGF-A is produced by the thyroid gland and as a result, the thyroid enlarges and the walls of the capillaries (constituted mainly by endothelial cells) increase the expression of VEGFR2, the receptor for VEGF-A. By blocking VEGFR2, IBS scientists could inhibit enlargement of the thyroid and stop vascular remodeling. "Our findings identify VEGFR2 blockade as a novel therapeutic avenue for targeting thyroid disease associated with thyrotropin," explains Koh. Concurrently, the research team could also exclude other molecular pathways. For example, they found that the angiopoietin-Tie2 pathway, fundamental in other tissues like the eyes and brain, does not play a major role in remodeling the vasculature of the thyroid gland. Finally, VEGFR3 was ruled out from the indispensable pool of proteins that maintain thyroid vascular integrity.


The present invention relates to a novel indene derivative, a preparation method for the same, and a pharmaceutical composition for preventing or treating retinal disease comprising the same as an active ingredient. The novel indene derivative of the present invention, the optical isomer of the same, or the pharmaceutically acceptable salts of the same have excellent inhibitory efficiency of receptor-interacting serine/threonine-protein kinase 1 (RIPK1). Therefore, the composition containing the same as an active ingredient can be effectively used as a pharmaceutical composition for preventing or treating retinal disease exemplified by retinitis pigmentosa (RP), Leber congenital amaurosis (LCA), Stargardts disease, Usher syndrome, choroideremia, rod-cone or cone-rod dystrophy, ciliopathy, mitochondrial disorders, progressive retinal atrophy, degenerative retinal diseases, age-related macular degeneration (AMD), wet AMD, dry AMD, geographical atrophy, inherited or acquired macular degeneration, retinal photoreceptor diseases, retinal pigment epithelial diseases, diabetic retinopathy, cystic macular edema, uveitis, retinal detachment, traumatic retinal injury, iatrogenic retinal injury, macular holes, macular capillarectasia, ganglion cell diseases, optic nerve diseases, glaucoma, optic neuropathy, ischemic retinal diseases, retinopathy of prematurity, occlusion of retinal vessels, inherited macroaneurysm, retinal vascular diseases, ophthalmic vascular diseases, glaucomatous retinal neurodegeneration, ischemic optic neuropathy and the like.


Zhang T.,Chungnam National University
Nature communications | Year: 2013

Constitutive NF-κB activation in cancer cells is caused by defects in the signalling network responsible for terminating the NF-κB response. Here we report that plant homeodomain finger protein 20 (PHF20) maintains NF-κB in an active state in the nucleus by inhibiting the interaction between PP2A and p65. We show that PHF20 induces canonical NF-κB signalling by increasing the DNA-binding activity of NF-κB subunit p65. In PHF20 overexpressing cells, the termination of tumour necrosis factor-induced p65 phosphorylation is impaired whereas upstream signalling events triggered by tumour necrosis factor are unaffected. This effect strictly depends on the interaction between PHF20 and methylated lysine residues of p65, which hinders recruitment of PP2A to p65, thereby maintaining p65 in a phosphorylated state. We further show that PHF20 levels correlate with p65 phosphorylation levels in human glioma specimens. Our work identifies PHF20 as a novel regulator of NF-κB activation and suggests that elevated expression of PHF20 may drive constitutive NF-κB activation in some cancers.


Patent
Samsung and Chungnam National University | Date: 2016-02-03

An apparatus of processing a signal or a biosignal, and a method of processing a signal or a biosignal are provided. The method of processing signal involves receiving a first reference signal having a frequency component of a measurement signal to be applied to a subject, receiving a second reference signal having a frequency component within a frequency bandwidth of an amplifier, and converting a first signal measured from the subject to a second signal within the frequency bandwidth of the amplifier, based on the first reference signal and the second reference signal.

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