Biomedical subjects

Min Jung Lee

Publications and source records attributed to Min Jung Lee.

9 recordsLinked to original sources

PubMed2006

Hydrophilic composite elastomeric mold for high-resolution soft lithography.

Here, we introduce a nanopatternable hydrophilic composite elastomer highly desirable for both nanostructure patterning via solvent-assisted micromolding (SAMIM) and microcontact printing of polar inks. This composite precursor is prepared by blending two UV-curable materials, Norland Optical Adhesives (NOA) 63 and poly(ethylene glycol) diacrylate (PEGDA), in an appropriate ratio; upon UV polymerization, a nanopatternable elastomer with preferential permeability both to aqueous and organic solvent is fabricated. Using this composite mold, nanoscale SAMIM of poly(4-vinylpyridine) (P4VP) and microcontact printing of a polar biomolecule, bovine serum albumin (BSA), was successfully demonstrated, paving the way for facile and efficient reproduction of various nanopatterns and a biomolecule-printed array platform.

Elastomers↗

PubMed2006

Multilayer transfer printing on microreservoir-patterned substrate employing hydrophilic composite mold for selective immobilization of biomolecules.

In this study, we introduce a hydrophilic composite mold with elasticity and moderate water permeability, suitable for transferring water-soluble polar molecules such as polyelectrolyte multilayer. This composite mold is constructed from two UV-curable polymers-Norland Optical Adhesives (NOA) 63, a urethane-related polymer, and poly(ethylene glycol) diacrylate (PEGDA). The mixture of inherently hard NOA 63 and hydrogel precursor, PEGDA, resulted in an optically transparent mold with some degree of elasticity and enhanced water permeability upon UV polymerization. Employing the NOA 63-PEGDA composite mold, a polyelectrolyte multilayer comprising alternate thin layers of poly(acrylic acid) (PAA) and poly(acrylamide) (PAAm) was transfer-printed onto arrays of microreservoir-patterned substrate to selectively prevent unwanted adsorption of biomolecules on the protruding surface. Antibody was immobilized selectively inside the microreservoirs where multilayer was not transferred, and a specific antibody binding reaction was detected inside the microreservoirs. Furthermore, the potential of this composite mold as a convenient tool for constructing a biosensor for detecting Escherichia coli (E. coli) O157:H7 was explored.

Antibodies↗

PubMed2006

Ecological hazard assessment of major veterinary benzimidazoles: acute and chronic toxicities to aquatic microbes and invertebrates.

Aquatic toxicities of six benzimidazole-based anthelmintics-namely, albendazole, thiabendazole, flubendazole, febantel, fenbendazole, and oxfendazole-were evaluated with a marine bacterium, Vibrio fischeri, and a freshwater invertebrate, Daphnia magna. Delayed and chronic toxicity tests using D. magna also were conducted for benzimidazoles with high acute toxicity. Vibrio fischeri was greater than 10-fold less sensitive to most of the benzimidazoles tested compared to daphnids. For D. magna, the most acutely toxic anthelmintic compound tested was fenbendazole (48-h median effective concentration [EC50s], 16.5 microg/L), followed by flubendazole (48-h EC50, 66.5 micro/L), albendazole (48-h EC50, 67.9 microg/L), febantel (48-h EC50, 216.5 microg/L), thiabendazole (48-h EC50, 843.6 microg/L), and oxfendazole (48-h EC50, 1,168.4 microg/L). The lipophilicity parameter, log Kow, explained the observed acute D. magna toxicity of the individual benzimidazoles (r = -0.91, p < 0.01). Delayed expression of toxicity observed for 21 d after 96-h exposure to fenbendazole and flubendazole was not notable, which might result from the relatively high elimination constants for the chemicals. With chronic exposure to fenbendazole, D. magna survival, reproduction, and growth were significantly impacted at 1.25 to 4.1 microg/L (p < 0.05). Hazard quotients estimated for fenbendazole, albendazole, flubendazole, and febantel were 2,770, 9.7, 4, and 1.2, respectively, suggesting a need for further investigation and a potential for environmental concerns, particularly with fenbendazole.

Animals↗

PubMed2005

Augmentation of UV-induced skin wrinkling by infrared irradiation in hairless mice.

Skin aging can be divided into intrinsic aging and photoaging. Sunlight is a major cause of photoaging, and is composed of ultraviolet (UV) and infrared (IR) radiation. Although the effects of UV radiation on skin aging have been widely studied, little is known about the biological effects of IR on the photoaging process in human skin. We found that chronic IR treatment induced wrinkles in hairless mice, and augments UV-induced wrinkle formation and UV-induced skin thickening in hairless mice. Histologically, we found that IR treatment augments UV-induced epidermal and dermal thickening, and that UV-induced increases of collagen and elastic fibers in dermis. Moreover, chronic IR treatment increased MMP-3 and MMP-13 mRNA expressions significantly in hairless mouse skin and augmented UV-induced MMP-3 and MMP-13 mRNA expressions and UV-induced MMP-2 and MMP-9 activities. From these results, we demonstrate that IR alone induces skin wrinkling and augments UV-induced wrinkle formation. Taken together, we suggest that IR plays an important role in the development of photoaging.

Animals↗

PubMed2004

Heat shock-induced matrix metalloproteinase (MMP)-1 and MMP-3 are mediated through ERK and JNK activation and via an autocrine interleukin-6 loop.

Although many studies have been performed to elucidate the molecular consequences of ultraviolet irradiation, little is known about the effect of infrared radiation on skin aging. In addition to photons, heat is likely to be generated as a consequence of infrared irradiation, and heat shock is widely considered to be an environmental stress. Here we investigated the effect of heat shock on the expressions of matrix metalloproteinase (MMP)-1, MMP-2, and MMP-3 in cultured human skin fibroblasts. Heat shock induced the expression of MMP-1 and MMP-3, but not MMP-2, at the mRNA and protein levels in a temperature-dependent manner, and caused the rapid activation of three distinct mitogen-activated protein kinases (MAPK), extracelluar signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. The heat shock-induced MMP-1 and MMP-3 expression was suppressed by the inhibition of ERK and JNK but not by p38 MAPK inhibition. Furthermore, heat shock increased the synthesis and release of interleukin-6 (IL-6) into culture media. The specific inhibition of IL-6 using a monoclonal antibody against IL-6 greatly reduced the expression of MMP-1 and MMP-3 induced by heat shock. Taken together, our results suggest that ERK and JNK play an important role in the induction of MMP-1 and MMP-3 by heat shock and that the heat shock-induced expression of MMP-1 and MMP-3 is mediated via an IL-6-dependent autocrine mechanism.

Antibodies↗

PubMed2002

Anti-apoptotic role of phospholipase D in spontaneous and delayed apoptosis of human neutrophils.

Neutrophil apoptosis is a constitutive process that can be enhanced or delayed by signals induced by various stimuli. We investigated the role of phospholipase D (PLD) in neutrophil apoptosis. The apoptotic rate of neutrophils was found to be increased by 1-butanol and decreased by the exogenous addition of PLD. Moreover, the delay of apoptosis by apoptosis-delaying stimuli such as granulocyte/macrophage colony-stimulating factor or lipopolysaccharide (LPS) was also blocked by 1-butanol. Unstimulated PLD activity in cultured cells for 20 h was higher than that in freshly isolated cells and further increased in cultured cells with LPS. These results suggest that PLD is involved in the up-regulation of neutrophil survival.

Adrenergic beta-Antagonists↗

PubMed2002

Activation of trkA induces differentiation and inhibits the growth of JK-GMS Askin tumor cells.

Peripheral primitive neuroectodermal tumor (PNET) and Ewing's sarcoma (ES) constitute a unique group of small round cell tumors in childhood and young adults that are characterized by the same chromosomal translocation t(11;22)(q24;q12). Recently, the expression of neurotrophin receptors has been found in various human tumors including PNET/ES, but the functional significance of these receptor expressions has not been documented in PNET/ES. In the present study, we investigated the biologic effects of trkA neurotrophin receptor activation by nerve growth factor (NGF) in a newly established Askin tumor cell line, JK-GMS, which constitutively expresses a high level of trkA. The activation of trkA induced differentiation and inhibited the growth of JK-GMS cells, which was characteristically associated with down-regulation of c-myc and N-myc mRNA expression. NGF did not exert significant changes in two different PNET/ES cell lines, CADO-ES1 and RD-ES, which did not express detectable levels of trkA. The biologic effects mediated by NGF were abrogated by treatment of the cells with K-252a, and the treatment with brain-derived neurotrophic factor did not affect the biologic behavior of JK-GMS cells, indicating that the effects are trkA specific. The results observed were quite similar to those of neuroblastoma cells, another childhood tumor of neural crest origin. Overall findings strongly suggest that the trkA-mediated signaling pathway plays a crucial role in controlling the basic biologic properties of JK-GMS cells.

Adolescent↗

PubMed2002

Saeng-Maek-San, a medicinal herb complex, protects liver cell damage induced by alcohol.

The effect of treatment with Saeng-Maek-San (SMS) Complex (SMS1 or SMS2) upon rat hepatocytes exposed to alcohol was investigated. We compared the serum biochemistry and liver histology of rats administered both alcohol and SMS to control rats treated with alcohol alone. SMS treatment resulted in a significant reduction in the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and triglycerides (TG) compared to the control rats. In contrast, expression levels of alcohol dehydrogenase (ADH) were increased. Electron microscopy indicated that administration of SMS preserved the structure of organelles, including the nucleus and mitochondria. In addition, lipid droplets and secondary lysosomes were observed in the control rats. These data suggest that SMS represents an excellent candidate for protection of rat hepatocytes from alcohol-mediated damage.

Animals↗

PubMedDate not supplied

Prevention of UV radiation-induced premature skin aging in hairless mice by the novel compound Melanocin A.

Repetitive exposure of the skin to UV radiation induces various harmful changes, such as thickening, wrinkle formation, inflammation and carcinogenesis. A variety of natural compounds and synthetic compounds have been studied to determine whether they can prevent UV-induced harmful effects. In this study, we investigated the effect of a novel compound, Melanocin A, which was isolated from Eupenicillium shearii F80695, on UV-induced premature skin aging. First, we studied the effect of Melanocin A on UV-induced matrix metalloproteinase (MMP)-9 expression in an immortalized human keratinocyte cell line, HaCaT, in vitro. Acute UV irradiation induced MMP-9 expression at both the mRNA and protein levels and Melanocin A suppressed this expression in a dose-dependent manner. We then investigated the effect of Melanocin A on UV-induced skin changes in hairless mice in vivo. Chronic exposure of hairless mouse dorsal skin to UV increased skin thickness and induced wrinkle formation and the gelatinase activities of MMP-2 and MMP-9. Moreover, Melanocin A significantly suppressed UV-induced morphologic skin changes and MMP-2 and MMP-9 expression. Taken together, these results show that Melanocin A can prevent the harmful effects of UV that lead to skin aging. Therefore, we suggest that Melanocin A should be viewed as a potential therapeutic agent for preventing and/or treating premature skin aging.

Animals↗