• JSTS:Journal of Semiconductor Technology and Science
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• v.13 no.6
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• pp.617-621
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• 2013

This study examined the effect of electron-beam (E-beam) irradiation on the electrical properties of n-GaN, AlGaN and AlGN/GaN structures on sapphire substrates. E-beam irradiation resulted in a significant decrease in the gate leakage current of the n-GaN, AlGaN and HEMT structure from $4.0{\times}10^{-4}A$, $6.5{\times}10^{-5}A$, $2.7{\times}10^{-8}A$ to $7.7{\times}10^{-5}A$, $7.7{\times}10^{-6}A$, $4.7{\times}10^{-9}A$, respectively, at a drain voltage of -10V. Furthermore, we also investigated the effect of E-beam irradiation on the AlGaN surface in AlGaN/GaN heterostructure high electron mobility transistors(HEMTs). The results showed that the maximum drain current density of the AlGaN/GaN HEMTs with E-beam irradiation was greatly improved, when compared to that of the AlGaN/GaN HEMTs without E-beam irradiation. These results strongly suggest that E-beam irradiation is a promising method to reduce leakage current of AlGaN/GaN HEMTs on sapphire through the neutralization the trap.

• BMB Reports
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• v.52 no.3
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• pp.214-219
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• 2019

The role of tumor-proximal factors in tumor plasticity during chemoresistance and metastasis following chemotherapy is well studied. However, the role of endothelial cell (EC) derived paracrine factors in tumor plasticity, their effect on chemotherapeutic outcome, and the mechanism by which these paracrine factors modulate the tumor microenvironment are not well understood. In this study, we report a novel mechanism by which endothelial miR-125a and let-7e-mediated regulation of interleukin-6 (IL-6) signaling can manipulate vasculogenic mimicry (VM) formation of MDA-MB-231 breast cancer cells. We found that endothelial IL-6 levels were significantly higher in response to cisplatin treatment, whereas levels of IL-6 upon cisplatin exposure remained unchanged in MDA-MB-231 breast cancer cells. We additionally found an inverse correlation between IL-6 and miR-125a/let-7e expression levels in cisplatin treated ECs. Interestingly, IL-6, IL-6 receptor (IL-6R), and signal transducer and activator of transcription 3 (STAT3) genes in the IL-6 pathway are closely regulated by miR-125a and let-7e, which directly target its 3' untranslated region. Functional analyses revealed that endothelial miR-125a and let-7e inhibit IL-6-induced adhesion of monocytes to ECs. Furthermore, conditioned medium from cisplatin treated ECs induced a significantly higher formation of VM in MDA-MB-231 breast cancer cells as compared to that from intact ECs; this effect of cisplatin treatment was abrogated by concurrent overexpression of miR-125a and let-7e. Overall, this study reveals a novel EC-tumor cell crosstalk mediated by the endothelial miR-125a/let-7e-IL-6 signaling axis, which might improve chemosensitivity and provide potential therapeutic targets for the treatment of cancer.

• Membrane Journal
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• v.11 no.4
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• pp.143-151
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• 2001

We have fabricated mixed-ionic conducting membranes, L $a_{0.6}$S $r_{0.4}$ $Co_{0.2}$F $e_{0.8}$ $O_{3-}$$\delta$/ and L $a_{0.7}$S $r_{0.3}$G $a_{0.6}$F $e_{0.4}$ $O_{3-}$$\delta$/ by the solid state method. Ceramic membranes consisted of perovskite-type structures and exhibited high relative density, >95%. Especially, dense L $a_{0.6}$S $r_{0.4}$Co $O_{3-}$$\delta$/ layer was coated on the L $a_{0.7}$S $r_{0.3}$G $a_{0.6}$F $e_{0.4}$ $O_{3-}$$\delta$/ membranes by using screen printing technique in order to improve oxygen ion flux. We measured oxygen ion flux on uncoated L $a_{0.6}$S $r_{0.4}$ $Co_{0.2}$F $e_{0.8}$ $O_{3-}$$\delta$/, uncoated L $a_{0.7}$S $r_{0.3}$G $a_{0.6}$F $e_{0.4}$ $O_{3-}$$\delta$/, and coated L $a_{0.7}$S $r_{0.3}$G $a_{0.6}$F $e_{0.4}$ $O_{3-}$$\delta$/ membranes. The L $a_{0.6}$S $r_{0.4}$ $Co_{0.2}$F $e_{0.8}$ $O_{3-}$$\delta$/ membranes showed the highest flux, 0.26 mL/min.$\textrm{cm}^2$ at 90$0^{\circ}C$, after steady state had been reached. The oxygen flux of coated L $a_{0.7}$S $r_{0.3}$G $a_{0.6}$F $e_{0.4}$ $O_{3-}$$\delta$/ membranes showed higher value, 0.19 mL/min.$\textrm{cm}^2$ at 95$0^{\circ}C$. This flux was as much as 2 or 3 times higher than those of uncoated L $a_{0.7}$S $r_{0.3}$G $a_{0.6}$F $e_{0.4}$ $O_{3-}$$\delta$/ membranes. 3-$\delta$/ membranes.X> 3-$\delta$/ membranes.membranes.

• Proceedings of the KSAR Conference
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• 2004.06a
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• pp.215-215
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• 2004

Human papillomavirus type 16 (HPV16) has been known as a major causative factor for the development of uterine cervical carcinomas. To investigate the in vivo activity of HPV16 expressed in squamous epithelia, transgenic mice harboring HPV16 E6/E7 with human keratin 14 (hK14) promoter were generated. Grossly, hK14 driven HPV16 E6/E7 transgenic mice exhibited multiple phenotypes, including wrinkled skin that was apparent prior to the appearance of hair in neonates, thickened ears, and loss of hair in adults. (omitted)

• YAKHAK HOEJI
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• v.44 no.4
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• pp.340-346
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• 2000

Cervical cancer is one of the leading causes of female death from cancer worldwide with about 500,000 deaths per year. A strong association between certain human papilloma viruses (HPV types 16 and 18) and cervical cancer has been well known. An extract of natural products, named as Somatid, has been used to investigate whether this agent has the ability of inhibiting the oncogenes E6 and E7 of HPV type 16. This Somatid inhibited the proliferation of human cervical cancer cell lines (C-33A, SiHa, CaSki) and HaCaT keratinocytes in a dose response manner, In vitro binding assay and ELISA showed that Somatid inhibited the in vitro biding of E6 and E6AP which are essential for the binding and degradation of the tumor suppressor p53. In addition, Somatid inhibited the in vitro binding of E7 and Rb which is essential tumor suppressor for the control of cell cycle. The levels of mRNA for E6 and E7 were also decreased by Somatid. Our data suggested that Somatid inhibited the oncogenecity of E6 and E7 of HPV 16 type, thus can be used as a putative anti-HPV agent for the treatment of cervical carcinomas caused by HPV.

• Journal of Microbiology and Biotechnology
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• v.17 no.7
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• pp.1169-1176
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• 2007

Genes encoding proteins responsible for limonene catabolism were cloned from a limonene-degrading microorganism, Enterobacter cowanii 6L, which was isolated from citron (Citrus junos) peel. The 8.6, 4.7, and 7.7 kb fragments (CD3, CD4, and CD6) of E. cowanii 6L chromosomal DNA that confer to E. coli the ability to grow on limonene have been cloned and their corresponding DNA sequences were determined. Nine open reading frames (ORFs) were identified, and the four ORFs (921 bp of CD3-2; 1,515 bp of CD4-1; 1,776 bp of CD6-1; and 1,356 bp of CD6-2) that encode limonene hydroxylase were confirmed by independently expressing these genes in E. coli. FAD and NADH were found to stimulate the hydroxylation reaction if added to cell extracts from E. coli recombinants, and multiple compounds (linalool, dihydrolinalool, perillyl alcohol, (${\alpha}-terpineol$, and ${\gamma}-terpineol$) were the principal products observed. Our results suggest that the isolate E. cowanii 6L has a broad metabolic capability including utilization of limonene. This broad metabolic ability was confirmed by identifying four novel limonene hydroxylase functional ORFs in E. cowanii 6L.

• Archives of Pharmacal Research
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• v.28 no.2
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• pp.172-176
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• 2005

Phytochemical investigation of the whole plant of Amberboa ramosa led to the isolation of six sesquiterpene lactones which could be identified as $8{\alpha}$-hydroxy-$11{\beta}$-methyl-$1{\alpha}H,\;5{\alpha}H,\;6{\beta}H,\;7{\alpha}H,\;11{\alpha}H-guai-10(14)$, 4(15)-dien-6, 12-olide(2), $3{\beta},\;8{\alpha}-dihydroxy-11{\alpha}-methyl-1{\alpha}H,\;5{\alpha}H,\;6{\beta}H,\;7{\alpha}H,\;11{\beta}H-guai-10(14)$, 4(15)-dien-6, 12-olide (2), $3{\beta},\;4{\alpha},\;8{\alpha}-trihydroxy-4{\beta}(hydroxymethyl)-1{\alpha}H,\;5{\alpha}H,\;6{\beta}H,\;7{\alpha}H-guai-10(14)$, 11(13)-dien-6, 12-olide (3), $3{\beta},\;4{\alpha},\;8{\alpha}-trihydroxy-4{\beta}-(chloromethyl)-1{\alpha}H,\;5{\alpha}H,\;6{\beta}H,\;7{\alpha}H-guai-10(14)$, 11(13)-dien-6, 12-olide(4), $3{\beta},\;4{\alpha},\;dihydroxy-4{\beta}-(hydroxymethyl)-1{\alpha}H,\;5{\alpha}H,\;6{\beta}H,\;7{\alpha}H-guai-10(14)$, 11(13)-dien-6, 12-olide(5), $3{\beta},\;4{\alpha}-dihydroxy-4{\beta}-(chloromethyl)-8{\alpha}-(4-hydroxymethacrylate)-1{\alpha}H,\;5{\alpha}H,\;6{\beta}H,\;7{\alpha}H-guai-10(14)$, 11(13)-dien-6, 12-olide (6) by spectroscopic methods. All of them showed inhibitory potential against butyrylcholinesterase.

• Proceedings of the KSAR Conference
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• 2003.06a
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• pp.45-45
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• 2003

Human papillomavirus type 16(HPV16) has been known to the major factor for the development of uterine cervical carcinomas. We have extended these studies to investigate the in vivo activities of HPV-16 E6/E7 when expressed in squamous epithelia of transgenic mice. Grossly, hK14HPV16E6/E7 transgenic mice had multiple phenotypes, including wrinkled skin that was apparent prior to the appearance of hair on neonates, thickened ears, and loss of hair in adults. In the transgenic mice, the wrinkled skin phenotype on the body and legs died at the age of 3∼4 weeks. Histological analysis of demonstrated that E6/E7 causes epidermal hyperplasia in multiple transgenic lineages with high penetrance. This epithelial hyperplasia was characterized by an expansion of the proliferating compartment and an expansion of the keratinocyte and was associated with hyperkeratosis. These transgenic mice expressed E6/E7 transgene mainly in skin, heart, pancreas and kidney. Hyperplasia was found at the skin. The enzyme activities of GR, GPx and CuZnSOD were measured from the transgene cause keratinocyte at the skin. The specific enzyme activities were significantly higher in transgenic mice skin compared to the normal mice skin. Thus these transgenic mice may be useful for the develpment of antioxidant enzymes or other therapies for HPV-associated hyperkeratosis.

• Microbiology and Biotechnology Letters
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• v.26 no.2
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• pp.89-95
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• 1998

Rhodopseudomonas sphaeroides K7 and E15-1 produced hydrogen from glucose rapidly for the first 24 hrs of culture under the anaerobic and photosynthetic conditions and then ceased the hydrogen production because of the accumulation of organic acids such as acetic acid and formic acid in the culture broth, decreasing the pH to 4.2-4.5. Only 43% and 73% of glucose in the culture were consumed even after 6 days of incubation by R. sphaeroides K7 and E15-1, respectively. The hydrogen production and glucose consumption, however, were substantially increased when the pH of the culture was adjusted to 6.8-7.0: Hydrogen production continues even after 10 days of culture and glucose was consumed completely after 2.5 and 4.5 days by R. sphaeroides K7 and E15-1, respectively, Furthermore, the bacteriochlorophyll contents in R. sphaeroides K7 and E15-1 were increased by 44 and 9 folds and the cell concentrations by 10 and 2.5 folds, respectively, after 7 days of culture. R. sphaeroides K7 and E15-1 also produced hydrogen from acetic, lactic, butyric and malic acids under the anaerobic and photosynthetic conditions even though the amounts of hydrogen produced were lower than that from glucose. The results of this experiment indicate that under the anaerobic and synthetic conditions R. sphaeroides K7 and E15-1 might use the NADH oxidation mediated by ferredoxin and hydrogenase to evolve hydrogen from glucose for the first 24 hrs and then the organic acids produced were used as electron donners for the production of hydrogen in the nitrogen-limited condition.

• YAKHAK HOEJI
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• v.46 no.6
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• pp.426-432
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• 2002

Cervical cancer is one of the leading causes of female death from cancer worldwide with about 500,000 deaths per year. A strong association between certain human papilloma viruses (HPV type 16 and 18) and cervical cancer has been well known. An extract of Saururus chinensis, named as PE-46, has been used to investigate whether this agent has the ability of inhibiting the oncogenes E6 and E7 of HPV type 16. PE-46 inhibited the proliferation of human cervical cancer cell lines in a dose response manner. PE-46 also inhibited the in vitro binding of E6 and E6AP which are essential for the binding and degradation of the tumor suppressor p53. In addition, PE-46 inhibited the in vitro binding of E7 and Rb which is essential tumor suppressor for the control of cell cycle. The levels of mRNA for E6 and E7 were also decreased by PE-46. SiHa cells treated with PE-46 induced G0/G1 arrest, resulting in inhibition of growth. Our study showed that the PE-46 can inhibit the cervical carcinomas via both inhibition of bindings between oncogenes and tumor suppressors, and inhibition of G1longrightarrowS transition. PE-46 inhibited the oncogenecity of E6 and E7 of HPV 16 type, thus could be used as a putative modulating agent for the treatment of cervical carcinomas caused by HPV.