• Korean Journal of Metals and Materials
• /
• v.46 no.8
• /
• pp.524-537
• /
• 2008

Zr-based amorphous alloy matrix composites reinforced with metallic continuous fibers were fabricated by liquid pressing process, and their fracture properties were investigated by directly observing microfracture process using an in situ loading stage installed inside a scanning electron microscope chamber. About 60 vol.% of metallic fibers were homogeneously distributed inside the amorphous matrix. Apparent fracture toughness of the stainless-steel- and tungsten-fiber-reinforced composites was lower than that of monolithic amorphous alloy, while that of the Ta-fiber-reinforced composite was higher. According to the microfracture observation, shear bands or cracks were initiated at the amorphous matrix, and the propagation of the initiated shear bands or cracks was effectively blocked by fibers, thereby resulting in stable crack growth which could be confirmed by the fracture resistance curve (R-curve) behavior. This increase in fracture resistance with increasing crack length improved fracture properties of the fiber-reinforced composites, and could be explained by mechanisms of formation of multiple shear bands or multiple cracks at the amorphous matrix and blocking of crack or shear band propagation and multiple necking at metallic fibers.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.2
• /
• pp.1017-1021
• /
• 2013

The cellular apoptosis susceptibility (CSE1L) gene has been demonstrated to regulate multiple cellular mechanisms including the mitotic spindle check point as well as proliferation and apoptosis. However, the importance of CSE1L in human colon cancer is largely unknown. In the present study, we examined expression levels of CSE1L mRNA by semiquantitative RT-PCR. A lentivirus-mediated small interfering RNA (siRNA) was used to knock down CSE1L expression in the human colon cancer cell line RKO. Changes in CSE1L target gene expression were determined by RT-PCR. Cell proliferation was examined by a high content screening assay. In vitro tumorigenesis was measured by colony-formation assay. Cell cycle distribution and apoptosis were detected by flow cytometric analysis. We found CSE1L mRNA to be expressed in human colon cancer cells. Using a lentivirus based RNAi approach, CSE1L expression was significantly inhibited in RKO cells, causing cell cycle arrest in the G2/M and S phases and a delay in cell proliferation, as well as induction of apoptosis and an inhibition of colony growth capacity. Collectively, the results suggest that silencing of CSE1L may be a potential therapeutic approach for colon cancer.

• Korean Journal of Materials Research
• /
• v.34 no.3
• /
• pp.152-162
• /
• 2024

In this study, we introduce a novel TiN/Ag embedded TiO₂/FTO resistive random-access memory (RRAM) device. This distinctive device was fabricated using an environmentally sustainable, solution-based thin film manufacturing process. Utilizing the peroxo titanium complex (PTC) method, we successfully incorporated Ag precursors into the device architecture, markedly enhancing its performance. This innovative approach effectively mitigates the random filament formation typically observed in RRAM devices, and leverages the seed effect to guide filament growth. As a result, the device demonstrates switching behavior at substantially reduced voltage and current levels, heralding a new era of low-power RRAM operation. The changes occurring within the insulator depending on Ag contents were confirmed by X-ray photoelectron spectroscopy (XPS) analysis. Additionally, we confirmed the correlation between Ag and oxygen vacancies (V_o). The current-voltage (I-V) curves obtained suggest that as the Ag content increases there is a change in the operating mechanism, from the space charge limited conduction (SCLC) model to ionic conduction mechanism. We propose a new filament model based on changes in filament configuration and the change in conduction mechanisms. Further, we propose a novel filament model that encapsulates this shift in conduction behavior. This model illustrates how introducing Ag alters the filament configuration within the device, leading to a more efficient and controlled resistive switching process.

• Journal of Microbiology and Biotechnology
• /
• v.18 no.2
• /
• pp.263-269
• /
• 2008

Hydrazinocurcumin (HC), a synthetic derivative of curcumin, has been reported to inhibit angiogenesis via unknown mechanisms. Understanding the molecular mechanisms of the drug's action is important for the development of improved compounds with better pharmacological properties. A genome-wide drug-induced haploinsufficiency screening of fission yeast gene deletion mutants has been applied to identify drug targets of HC. As a first step, the 50% inhibition concentration $(IC_{50})$ of HC was determined to be $2.2{\mu}M$. The initial screening of 4,158 mutants in 384-well plates using robotics was performed at concentrations of 2, 3, and $4{\mu}M$. A second screening was performed to detect sensitivity to HC on the plates. The first screening revealed 178 candidates, and the second screening resulted in 13 candidates, following the elimination of 165 false positives. Final filtering of the condition-dependent haploinsufficient genes gave eight target genes. Analysis of the specific targets of HC has shown that they are related to septum formation and the general transcription processes, which may be related to histone acetyltransferase. The target mutants showed 65% growth inhibition in response to HC compared with wild-type controls, as shown by liquid culture assay.

• Journal of Ginseng Research
• /
• v.48 no.1
• /
• pp.31-39
• /
• 2024

Background: Ginsenoside Rg3, a primary bioactive component of red ginseng, has anti-cancer effects. However, the effects of Rg3-enriched ginseng extract (Rg3RGE) on apoptosis and autophagy in breast cancer have not yet been investigated. In the present study, we explored the anti-tumor effects of Rg3RGE on breast cancer cells stimulated CoCl₂, a mimetic of the chronic hypoxic response, and determined the operative mechanisms of action. Methods: The inhibitory mechanisms of Rg3RGE on breast cancer cells, such as apoptosis, autophagy and ROS levels, were detected both in vitro. To determine the anti-cancer effects of Rg3RGE in vivo, the cancer xenograft model was used. Results: Rg3RGE suppressed CoCl₂-induced spheroid formation and cell viability in 3D culture of breast cancer cells. Rg3RGE promoted apoptosis by increasing cleaved caspase 3 and cleaved PARP and decreasing Bcl2 under the hypoxia mimetic conditions. Further, we identified that Rg3RGE promoted apoptosis by inhibiting lysosomal degradation of autophagosome contents in CoCl₂-induced autophagy. We further identified that Rg3RGE-induced apoptotic cell death and autophagy inhibition was mediated by increased intracellular ROS levels. Similarly, in the in vivo xenograft model, Rg3RGE induced apoptosis and inhibited cell proliferation and autophagy. Conclusion: Rg3RGE-stimulated ROS production promotes apoptosis and inhibits protective autophagy under hypoxic conditions. Autophagosome accumulation is critical to the apoptotic effects of Rg3RGE. The in vivo findings also demonstrate that Rg3RGE inhibits breast cancer cell growth, suggesting that Rg3RGE has potential as potential as a putative breast cancer therapeutic.

• Journal of the Korea Academia-Industrial cooperation Society
• /
• v.10 no.10
• /
• pp.2990-2996
• /
• 2009

S. mutans, one of a major causal agents of dental caries, is component of the dental plaque and produces various organic acids such as lactic acid as the end-product of glycolysis. In this study, we are interested in comparing the gene expression of acid-shocked and control cells of S. mutans isolated from Korean with caries. Expression levels of gtfB, gtfC, gtfD and ftf were analyzed by Real-time PCR, when the cells were grown under 20 mM lactic acid stress in the exponential phase. The data showed reduced expression of these genes. S. mutans is known to have developed a variety of mechanisms to tolerate acid sterss. A more detailed analysis of the functions and interactions of acid stress proteins connecting the growth, stress tolerance, biofilm formation is under way.

• Asian Pacific Journal of Cancer Prevention
• /
• v.16 no.2
• /
• pp.627-633
• /
• 2015

Background: To study the effect of parecoxib, a novel cyclooxygenase-2 selective inhibitor, on the radiation response of colorectal cancer (CRC) cells and its underlying mechanisms. Materials and Methods: Both in vitro colony formation and apoptosis assays as well as in vivo mouse xenograft experiments were used to explore the radiosensitizing effects of parecoxib in human HCT116 and HT29 CRC cells. Results: Parecoxib sensitized CRC cells to radiation in vitro with a sensitivity enhancement ratio of 1.32 for HCT116 cells and 1.15 for HT29 cells at a surviving fraction of 0.37. This effect was partially attributable to enhanced apoptosis induction by parecoxib combined with radiation, as illustrated using an in vitro apoptosis assays. Parecoxib augmented the tumor response of HCT116 xenografts to radiation, achieving growth delay more than 20 days and an enhancement factor of 1.53. In accordance with the in vitro results, parecoxib combined with radiation resulted in less proliferation and more apoptosis in tumors than radiation alone. Radiation monotherapy decreased microvessel density (MVD) and microvessel intensity (MVI), but increased the hypoxia level in xenografts. Parecoxib did not affect MVD, but it increased MVI and attenuated hypoxia. Conclusions: Parecoxib can effectively enhance radiation sensitivity in CRC cells through direct effects on tumor cells and indirect effects on tumor vasculature.

• Proceedings of the Plant Resources Society of Korea Conference
• /
• 2019.04a
• /
• pp.111-111
• /
• 2019

Glycyrrhizae radix is one of the most frequently prescribed ingredients in Oriental medicine, and G. radix extract has been shown to exert anti-cancer effects. However, the cellular and molecular mechanisms of apoptosis by G. radix are poorly defined. In the present study, it was examined the biochemical mechanisms of apoptosis by water extract of G. radix (WEGR) in human bladder T24 cancer cells. It was found that WEGR could inhibit the cell growth of T24 cells in a dose-dependent manner, which was associated with the induction of apoptotic cell death, as evidenced by the formation of apoptotic bodies, DNA fragmentation and increased populations of annexin-V positive cells. The induction of apoptotic cell death by WEGR was connected with an up-regulation of pro-apoptotic Bax protein expression and down-regulation of anti-apoptotic Bcl-2 and Bcl-xL proteins, and inhibition of apoptosis family proteins (XIAP, cIAP-1 and cIAP-2). In addition, apoptosis-inducing concentrations of WEGR induced the activation of caspase-9, an initiator caspase of the mitochondrial-mediated intrinsic pathway, and caspase-3, accompanied by proteolytic degradation of poly (ADP-ribose)-polymerase. WEGR also induced apoptosis via a death receptor-mediated extrinsic pathway by caspase-8 activation, resulting in the down-regulation of total Bid and suggesting the existence of cross-talk between the extrinsic and intrinsic pathways. Taken together, the present results suggest that WEGR may be a potential chemotherapeutic agent for the control of human bladder cancer cells.

• The Korean Journal of Physiology and Pharmacology
• /
• v.26 no.6
• /
• pp.479-499
• /
• 2022

The lack of a clonal renin-secreting cell line has greatly hindered the investigation of the regulatory mechanisms of renin secretion at the cellular, biochemical, and molecular levels. In the present study, we investigated whether it was possible to induce phenotypic switching of the renin-expressing clonal cell line As4.1 from constitutive inactive renin secretion to regulated active renin secretion. When grown to postconfluence for at least two days in media containing fetal bovine serum or insulin-like growth factor-1, the formation of cell-cell contacts via N-cadherin triggered downstream cellular signaling cascades and activated smooth muscle-specific genes, culminating in phenotypic switching to a regulated active renin secretion phenotype, including responding to the key stimuli of active renin secretion. With the use of phenotype-switched As4.1 cells, we provide the first evidence that active renin secretion via exocytosis is regulated by phosphorylation/dephosphorylation of the 20 kDa myosin light chain. The molecular mechanism of phenotypic switching in As4.1 cells described here could serve as a working model for full phenotypic modulation of other secretory cell lines with incomplete phenotypes.

• Korean Journal of Environmental Biology
• /
• v.17 no.1
• /
• pp.1-9
• /
• 1999

Numerous observations revealed strong evidence of increased middle ultraviolet radiation or UV-B (280 ~ 320 nm) at the earth's surface resulting from stratospheric ozone depletion. UV is the waveband of electromagnetic radiation which is strongly absorbed by nucleic acids and proteins, thus causing damage to living systems. It has been recorded in the East Sea, Korea that solar UV-B impinging on the ocean surface penetrates seawater to significant depths. Recent researches showed that exposure to UV-B for as short as 2h at the ambient level (2.0 Wm$^{-2}$) decreased macroalgal growth and photosynthesis and destroyed photosynthetic pigments. These may suggest that UV-B could be an important environmental factor to determine algal survival and distribution. Some adaptive mechanisms to protect macroalgae from UV-damage have been found, which include photoreactivation and formation of UV-absorbing pigments. Post-illumination of visible light mitigated UV-induced damage in laminarian young sporophytes with blue the most effective waveband. The existence of UV-B absorbing pigments has been recognized in the green alga, Ulva pertusa and the red alga, Pachymeniopsis sp., which is likely to exert protective function for photosynthetic pigments inside the thalli from UV-damage. Further studies are however needed to confirm that these mechanisms are of general occurrence in seaweeds. Macroalgae together with phytoplankton are the primary producers to incorporate about 100 Gt of carbons per year, and provide half of the total biomass on the earth. UV-driven reduction in macroalgal biomass, if any, would therefore cause deleterious effects on marine ecosystem. The ultimate impacts of increasing UV-B flux due to ozone destruction are still unknown, but the impression from UV studies made so far seems to highlight the importance of setting up long-term monitoring system for us to be able to predict and detect the onset of large -scale deterioration in aquatic ecosystem.