Han-Sol Jeong

Friction and thermal phenomena in chemical mechanical polishing

Abstract The friction and thermal phenomenon was investigated to verify the effect of temperature on the material removal mechanism in chemical mechanical polishing (CMP). To this end, the polishing of various materials, temperature measurement by way of infrared ray camera, frictional force measurement and real contact area measurement experiment were conducted. From the results of these experiments, we concluded that the material removal mechanism in CMP under the influence of increasing temperature, is dominated by the increase in chemical reactions rather than mechanical ones. Furthermore, the removal rate did not remain constant during the polishing process and this has an effect on the within wafer non-uniformity (WIWNU).

Time-Dependent Control of Hole-Opening Degree of Porous ZnO Hollow Microspheres

Well-designed, monodispersed porous ZnO hollow microspheres with controlled hole-opening were successfully synthesized by a facile two-step solution route at low temperature. The hollow microspheres having average diameter of 3-4 μm showed time-dependent hole-opening, i.e. 4-100% for 15-75 min. The hole-opening percentage increases linearly with time until complete opening. The ZnO hollow microspheres also exhibited a high surface area (34 m(2) g(-1)), a large pore volume (0.19 cm(3) g(-1)) and an average pore diameter of 3.8 nm. A plausible growth mechanism for the formation of ZnO hollow microspheres was also proposed.

A comprehensive in vitro and in vivo study of ZnO nanoparticles toxicity

Nowadays, the exploration of zinc oxide nanoparticles (ZnO NPs) based products is booming in the various directions of bio-nanomedicine and other consumer products, but the comprehensive toxicological impact posed by ZnO NPs still remains unclear. The present study systematically investigates and correlates the toxicity evaluation of ZnO NPs in RAW 264.7 murine macrophages (in vitro) and male ICR mice (in vivo) by two different administration routes, i.e. g.i. and i.p. at different doses. The in vitro studies showed a slight rise in intracellular reactive oxygen species level (ROS), NF-κB transcription factor expression (TF) and NPs uptake at higher dose, indicating the non-toxic nature of ZnO NPs below 100 μg mL-1 doses. The in vivo results demonstrate a slight gain in body weight (BW), reduction in the organ weight, mild to severe pathological alteration in the organs depending upon NP dosage and mode of administration routes. The histopathological investigation suggests that the liver, kidney, lung, spleen, and pancreas may be the target organs for ZnO NPs according to the administration routes. Serum biochemistry assay shows an elevation in the GPT and ALP level, suggesting liver dysfunction. To our knowledge, this is the first study to report the toxic effects of ZnO NPs through i.p. administration. Further, the present work will offer a deeper understanding regarding the toxicology and in vivo behaviours of ZnO NPs in mice depending upon the various administration routes.

Effect of ZnO nanoparticles aggregation on the toxicity in RAW 264.7 murine macrophage

Nanostructured zinc oxide (ZnO) has received much attention due to its biological and medical applications, where detailed knowledge about particle sizing, aggregation propensity and its related hazards are crucial. Herein, the aggregation propensity and dissolution behavior of ZnO nanoparticles in aqueous medium (PBS) were studied as a function of concentration and further correlated with its toxicity in RAW 264.7 murine macrophages. Fast formation of smaller aggregates having high dissolution rate was observed at low concentration ZnO (LC-ZnO). Compared to high concentration ZnO (HC-ZnO) aggregates, the LC-ZnO aggregates were highly pronounced in terms of reactive oxygen species generation and exerting cell apoptosis, ascribed to the secondary size effect, size-dependent cellular uptake and ion solubility. This study outlines the nanoparticle concentration as a key factor in scaling its aggregation, dissolution tendency and also emphasizes the accounting of ingested nanomaterials long-term fate inside the cells.

Rehmannia glutinosa suppresses inflammatory responses elicited by advanced glycation end products.

Fresh rhizome of Rehmannia glutinosa Libosch. (Saeng-jihwang in Korean: SJH) has been prescribed for the treatment of diabetes-associated complications. The purpose of the present study is to investigate the underlying mechanisms of the efficacy of SJH in diabetes-related complications. Decoction was obtained after boiling SJH in water and subsequent lyophilization. The cellular toxicity of SJH was determined by MTT assay. The antioxidant activity of SJH was measured by DPPH and DCFH-DA assays. The effects of SJH on inflammatory responses elicited by AGEs were assessed by western blotting and semi-quantitative RT-PCR analyses. The water extract of SJH had a high free radical scavenging activity in vitro and decreased the level of intracellular ROS in THP-1 cells treated with AGEs. SJH suppressed the expression of pro-inflammatory genes, including TNF-α, MCP-1, IP-10, COX-2, and iNOS; the activation of NF-κB; and the expression of RAGE, a receptor for AGEs, where the expressions of which were induced by AGEs. These results suggest the possibility that SJH can be an alternative therapeutics for diabetes-associated diseases.

Caffeic Acid Phenethyl Ester Inhibits Alpha-Melanocyte Stimulating Hormone-Induced Melanin Synthesis through Suppressing Transactivation Activity of Microphthalmia-Associated Transcription Factor

Caffeic acid phenethyl ester (1), a natural compound found in various plants and propolis, is a well-known anti-inflammatory, immunomodulatory, and cytotoxic agent. The present study aimed to investigate the molecular events underlying the antimelanogenic activity of 1 in alpha-melanocyte stimulating hormone (α-MSH)-stimulated B16-F10 melanoma cells. In this investigation, 1 effectively reduced α-MSH-stimulated melanin synthesis by suppressing expression of melanogenic enzymes such as tyrosinase, tyrosinase-related protein-1 (TRP-1), and tyrosinase-related protein-2 (TRP-2), although this compound did not directly inhibit tyrosinase enzyme activity. On the other hand, the expression and nuclear translocation of microphthalmia-associated transcription factor (MITF) as a key transcription factor for tyrosinase expression regulating melanogenesis were not affected by treatment with 1. The upstream signaling pathways including cAMP response element-binding protein (CREB), glycogen synthase kinase-3β (GSK-3β), and Akt for activation and expression of MITF were also not influenced by 1. Interestingly, 1 inhibited transcriptional activity of a tyrosinase promoter by suppressing the interaction of MITF protein with an M-box containing a CATGTG motif on the tyrosinase promoter. Given the important role of MITF in melanogenesis, suppression of 1 on the function of MITF to transactivate tyrosinase promoter may present a novel therapeutic approach to treat hyperpigmentation disorders.

Intelligently automated polishing for high quality surface formation of sculptured die

Abstract An intelligent polishing system that improves the surface quality of sculptured die surfaces on a 5-axis polishing machine including a pneumatic polishing head is proposed. In general, a mechanically automated polishing system has the critical drawback of not being able to adjust polishing conditions as adequately as an experienced operator can. One of the main reasons is that the system does not have sensors equal to human fingers that can adapt to the changing conditions of the polished surface. In the proposed system, acoustic emission (AE) sensors are adopted to detect even a tiny change of the polishing status. Based on the on-site status information, polishing conditions such as pressure, feed rate and tool mesh are adjusted in process to achieve better surface quality as fast as possible using an AE-based intelligent monitoring scheme.

Catalpol suppresses advanced glycation end-products-induced inflammatory responses through inhibition of reactive oxygen species in human monocytic THP-1 cells.

Advanced glycation end-products (AGEs) play a pivotal role in the development of diabetic complications by inducing inflammation. We previously reported that the fresh roots of Rehmannia glutinosa Libosch., which have been used for the treatment of diabetes in traditional Korean medicine, also have the potential to suppress AGE-mediated inflammatory response in THP-1 cells. In the present study, we isolated catalpol from R. glutinosa, and examined whether it has anti-inflammatory effects on AGE-stimulated THP-1 cells. Catalpol reduced the expression of pro-inflammatory mediates, such as monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-α (TNF-α), inducible NO synthase (iNOS), and receptor for AGE (RAGE). Promoter and electromobility shift assays showed that transcriptional activation of NF-κB was significantly reduced by catalpol treatment, while AP-1 was not. Catalpol also suppressed AGE-induced phosphorylation of mitogen activated protein (MAP) kinases, degradation of IκBα and the nuclear localization of NF-κB. Moreover, the production of intracellular reactive oxygen species (ROS) elicited by AGE was also suppressed by catalpol treatment, through dual action of reducing ROS itself and inhibiting NADPH oxidase activity. Our findings indicate that catalpol suppresses AGE-mediated inflammation by inhibiting ROS production and NF-κB activity. We suggest that catalpol, a major constituent of the fresh roots of R. glutinosa, contributes to the prevention of AGE-mediated diabetic complications.

Marine algal fucoxanthin inhibits the metastatic potential of cancer cells

Metastasis is major cause of malignant cancer-associated mortality. Fucoxanthin has effect on various pharmacological activities including anti-cancer activity. However, the inhibitory effect of fucoxanthin on cancer metastasis remains unclear. Here, we show that fucoxanthin isolated from brown alga Saccharina japonica has anti-metastatic activity. To check anti-metastatic properties of fucoxanthin, in vitro models including assays for invasion, migration, actin fiber organization and cancer cell-endothelial cell interaction were used. Fucoxanthin inhibited the expression and secretion of MMP-9 which plays a critical role in tumor invasion and migration, and also suppressed invasion of highly metastatic B16-F10 melanoma cells as evidenced by transwell invasion assay. In addition, fucoxanthin diminished the expressions of the cell surface glycoprotein CD44 and CXC chemokine receptor-4 (CXCR4) which play roles in migration, invasion and cancer-endothelial cell adhesion. Fucoxanthin markedly suppressed cell migration in wound healing assay and inhibited actin fiber formation. The adhesion of B16-F10 melanoma cells to the endothelial cells was significantly inhibited by fucoxanthin. Moreover, in experimental lung metastasis in vivo assay, fucoxanthin resulted in significant reduction of tumor nodules. Taken together, we demonstrate, for the first time, that fucoxanthin suppresses metastasis of highly metastatic B16-F10 melanoma cells in vitro and in vivo.

Protective Effect of the Fruit Hull of Gleditsia sinensis on LPS-Induced Acute Lung Injury Is Associated with Nrf2 Activation

The fruit hull of Gleditsia sinensis (FGS) has been prescribed as a traditional eastern Asian medicinal remedy for the treatment of various respiratory diseases, but the efficacy and underlying mechanisms remain poorly characterized. Here, we explored a potential usage of FGS for the treatment of acute lung injury (ALI), a highly fatal inflammatory lung disease that urgently needs effective therapeutics, and investigated a mechanism for the anti-inflammatory activity of FGS. Pretreatment of C57BL/6 mice with FGS significantly attenuated LPS-induced neutrophilic lung inflammation compared to sham-treated, inflamed mice. Reporter assays, semiquantitative RT-PCR, and Western blot analyses show that while not affecting NF-κB, FGS activated Nrf2 and expressed Nrf2-regulated genes including GCLC, NQO-1, and HO-1 in RAW 264.7 cells. Furthermore, pretreatment of mice with FGS enhanced the expression of GCLC and HO-1 but suppressed that of proinflammatory cytokines in including TNF-α and IL-1β in the inflamed lungs. These results suggest that FGS effectively suppresses neutrophilic lung inflammation, which can be associated with, at least in part, FGS-activating anti-inflammatory factor Nrf2. Our results suggest that FGS can be developed as a therapeutic option for the treatment of ALI.