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Incheon, South Korea

Lee N.Y.,Gachon University | Lee N.Y.,Gachon Medical Research Institute
Colloids and Surfaces B: Biointerfaces | Year: 2013

In this study, a simple and facile scheme for selectively hydrophobizing microwell-patterned hydrophilic polymer substrate is demonstrated, and applied for a targeted adhesion. Microwell-patterned polymer substrate was replicated from a silicon mold using a photocurable prepolymer under ultraviolet (UV) light for 30. min. While the surface of the replica was partially cured, it was contact printed with a flat, hydrophobic poly(dimethylsiloxane) (PDMS) elastomer, and the assembly was further cured under UV light for approximately 3. h and detached. In this manner, the PDMS molecules were transferred selectively onto the protruding regions of the partially cured microwell-patterned substrate, while the inner walls of the microwells remained hydrophilic. The surface hydrophobization was characterized by contact angle measurement and X-ray photoelectron spectroscopy (XPS). In addition, time-dependent contact angle variations were investigated to verify the robustness and durability of the coating of the PDMS functional group. As a proof-of-concept experiment, functionalized polymer beads were targeted and successfully guided selectively into arrays of microwells without being adsorbed onto the protruding regions of the microwell-patterned substrate, which could further be applied for the targeted immobilization of biomolecules with high selectivity in a relatively simple and facile manner. © 2013 Elsevier B.V. Source


Oh Y.S.,Gachon University | Oh Y.S.,Gachon Medical Research Institute
Anatomy and Cell Biology | Year: 2015

Pancreatic islets are responsible for blood glucose homeostasis. Reduced numbers of functional (insulin-secreting) beta-cells in pancreatic islets underlies diabetes. Restoration of the secretion of the proper amount of insulin is a goal. Beta-cell mass is increased by neogenesis, proliferation and cell hypertrophy, and is decreased by beta-cell death primarily through apoptosis. Many hormones and nutrients affect beta-cell mass, and glucose and free fatty acid are thought to be the most important determinants of beta-cell equilibrium. A number of molecular pathways have been implicated in beta-cell mass regulation and have been studied. This review will focus on the role of the principle metabolites, glucose and free fatty acid, and the downstream signaling pathways regulating beta-cell mass by these metabolite. © 2015. Source


Oh Y.S.,Gachon University | Oh Y.S.,Gachon Medical Research Institute | Lee Y.-J.,Gachon University | Kang Y.,Ajou University | And 3 more authors.
Journal of Endocrinology | Year: 2013

Prolonged exposure to high glucose (HG) and palmitate (PA) results in increased ER stress and subsequently induces β-cell apoptosis. Exendin-4, a glucagon-like peptide-1 agonist, is known to protect β cells from toxicity induced by cytokines, HG, or fatty acids by reducing ER stress. However, the detailed molecular mechanisms for this protective effect are still not known. In this study, we investigated the role of exendin-4 in the inhibition of glucolipotoxicity-induced ER stress and β-cell apoptosis. Exendin-4 treatment protected INS-1 β cells from apoptosis in response to HG/PA (25 mM glucoseC400 μM PA). HG/PA treatment increased cleaved caspase-3 and induced ER stress maker proteins such as PERK (EIF2AK3), ATF6, and phosphorylated forms of PERK, eIF2α, IRE1α (ERN1), and JNK (MAPK8), and these increases were significantly inhibited by exendin-4 treatment. HG/PA treatment of INS-1 cells increased SREBP1 (SREBF1) protein and induced its nuclear translocation and subsequently increased C/EBPβ (CEBPB) protein and its nuclear translocation. Exendin-4 treatment attenuated this increase. Knockdown of SREBP1c reduced the activation of C/EBPβ and also blocked the expression of ER stress markers induced by HG/PA treatment. Our results indicate that exendin-4 inhibits the activation of SREBP1c and C/EBPβ, which, in turn, may reduce glucolipotoxicity-induced ER stress and β-cell apoptosis. © 2013 Society for Endocrinology. Source


Jang M.,Gachon University | Park C.K.,Gachon University | Lee N.Y.,Gachon University | Lee N.Y.,Gachon Medical Research Institute
Sensors and Actuators, B: Chemical | Year: 2014

In this paper, we introduce a simple strategy for modifying the surface of polycarbonate (PC) to make it either hydrophilic or hydrophobic. The aminosilane, bis[3-(trimethoxysilyl)propyl]amine (bis-TPA), was used to produce the hydrophilic surface via aminolysis of the carbonate backbone to form strong urethane linkages, leaving alkoxysilane parts exposed on the surface. To obtain the hydrophobic surface, PC coated with bis-TPA was further reacted with (tridecafluoro-1,1,2,2-tetrahydrooctyl)-triethoxysilane (FTES), where inorganic moieties of both silanes condensed to realize siloxane (Si-O-Si) bonds. In this way, fluorinated groups were left exposed on the terminal surface of the PC, rendering it hydrophobic. In-depth surface characterizations were performed, including water contact angle measurement and X-ray photoelectron spectroscopy (XPS) analysis, in order to identify the optimum conditions for achieving surface modification without sacrificing substrate transparency. To extend the use of these PC surface treatments to microfluidic applications, the hydrophilic coating was further adopted for use in bonding two PC substrates by forming Si-O-Si bonds at the interface. Using the hydrophilic treatment of PC, we obtained microchannels, which were resistant to organic solvents. Furthermore, by employing subsequent hydrophobic treatment, multiple liquids were successfully injected into microchannels sequentially in a valve-free manner © 2013 Elsevier B.V. Source


Trinh K.T.L.,Gachon University | Wu W.,Gachon University | Lee N.Y.,Gachon University | Lee N.Y.,Gachon Medical Research Institute
Sensors and Actuators, B: Chemical | Year: 2014

In this study, we fabricate a hybrid planar microdevice to perform an on-chip flow-through polymerase chain reaction (PCR) constructed by assembling glass and poly(dimethylsiloxane) (PDMS) on which a serpentine microchannel is engraved. The proposed system employs a metal alloy slab, called Invar, which is basically a nickel iron alloy, sandwiched between the microdevice and a heater. Owing to the high thermal conductivity (10 W K-1 m-1) but notably low thermal expansion coefficient (1.6 × 10-6 K -1) of Invar, a stable temperature gradient was established on its surface. The Invar was placed on the heater in such a way that they made partial contact, with the rest of the Invar exposed to the air. A uniformly distributed temperature gradient, which ranged in temperatures from 57 C to 95 C, was first established on the Invar sheet, and a planar microdevice was directly placed atop the Invar sheet. The proposed system was successfully applied to amplify three targets: a 230 bp gene fragment from a plasmid vector, the first 282 bp of the interferon-beta (IFN-β) promoter from human genomic DNA, and a 409 bp long gene fragment in thyroid transcription factor-1 (TTF-1), which is used effectively as a marker for diagnosing lung and thyroid carcinomas, from human genomic DNA. All of the targets were amplified within less than 30 min. One microdevice was utilized repeatedly for multiple target amplifications by fine tuning the relative position of the Invar sheet on the heater. © 2013 Elsevier B.V. All rights reserved. Source

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