• Journal of the Korean institute of surface engineering
• /
• v.54 no.6
• /
• pp.307-314
• /
• 2021

Diamond-like carbon (DLC) is difficult to achieve sufficient adhesion because of weak bonding between DLC film and the substrate. The purpose of this study is to improve the adhesion between substrate and DLC film. DLC film was deposited on AISI H13 using linear ion source. To improve adhesion, the substrate was treated by dual post plasma nitriding. In order to define the mechanism of the improvement in adhesive strength, the gradient layer between substrate and DLC film was analyzed by Glow Discharge Spectrometer (GDS) and Scanning Electron Microscope (SEM). The microstructure of the DLC film was analyzed using a micro Raman spectrometer. Mechanical properties were measured by nano-indentation, micro vickers hardness tester and tribology tester. The characteristic of adhesion was observed by scratch test. The adhesion of the DLC film was enhanced by active screen plasma nitriding layer.

• YAKHAK HOEJI
• /
• v.52 no.5
• /
• pp.412-417
• /
• 2008

BAY11-7082 was initially found to be an anti-inflammatory drug with NF-${\kappa}B$ inhibitory property. In this study, we evaluated modulatory function of BAY11-7082 on U937 cell-cell adhesion induced by CD29 (${\beta}1$-integrins). BAY11-7082 strongly blocked functional activation of CD29 (${\beta}1$-integrins), as assessed by cell-cell adhesion assay. However, this compound did not block a simple activation of CD29, as assessed by cell-fibronectin adhesion assay. In particular, to understand molecular mechanism of BAY11-7082-mediated inhibition, the regulatory roles of CD29-induced actin cytoskeleton rearrangement under cell-cell adhesion and surface level of CD29 were examined using confocal and flow cytometic analysis. Interestingly, this compound strongly suppressed the molecular association of actin cytoskeleton with CD29 at cell-cell adhesion site. Moreover, BAY11-7082 also diminished surface levels of CD29 as well as its-associated adhesion molecule CD147, but not other adhesion molecules such as CD18 and CD43. Therefore, our data suggest that BAY11-7082 may be involved in regulating immune responses managed by CD29-mediated cell-cell adhesion.

• The Journal of Korea Robotics Society
• /
• v.5 no.3
• /
• pp.177-185
• /
• 2010

In this paper, a wall climbing robot, called LAVAR, is developed, which is using an impeller for adhering. The adhesion mechanism of the robot consists of an impeller and two-layered suction seals which provide sufficient adhesion force for the robot body on the non smooth vertical wall and horizontal ceiling. The robot uses two driving-wheels and one ball-caster to maneuver the wall surface. A suspension mechanism is also used to overcome the obstacles on the wall surface. For its design, the whole adhering mechanism is analyzed and the control system is built up based on this analysis. The performances of the robot are experimentally verified on the vertical and horizontal flat surfaces.

• The Korean Journal of Physiology and Pharmacology
• /
• v.12 no.5
• /
• pp.231-236
• /
• 2008

Heparin is a well-known anticoagulant widely used in various clinical settings. Interestingly, recent studies have indicated that heparin also has anti-inflammatory effects on neuroinflammation-related diseases, such as Alzheimer's disease and meningitis. However, the underlying mechanism of its actions remains unclear. In the present study, we examined the anti-inflammatory mechanism of heparin in cultured cerebral endothelial cells (CECs), and found that heparin inhibited the tumor necrosis factor $\alpha$ ($TNF{\alpha}$)-induced and nuclear factor kappa B (NF-${\kappa}B$)-dependent expression of adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), which are crucial for inflammatory responses. Heparin selectively interfered with NF-${\kappa}B$ DNA-binding activity in the nucleus, which is stimulated by $TNF{\alpha}$. In addition, non-anticoagulant 2,3-O desulfated heparin (ODS) prevented NF-${\kappa}B$ activation by $TNF{\alpha}$, suggesting that the anti-inflammatory mechanism of heparin action in CECs lies in heparin's ability to inhibit the expression of cell adhesion molecules, as opposed to its anticoagulant actions.

• Elastomers and Composites
• /
• v.54 no.4
• /
• pp.299-307
• /
• 2019

Rubber friction properties include adhesion friction characteristics of the interface, hysteresis friction characteristics originating from repeated rubber deformations, and cohesion friction characteristics due to wear and tear. Cohesion friction is generally sufficiently small (< 3%) that it can be ignored, whereas adhesion friction has a relatively large contribution of 15%, but has not been investigated thoroughly. Therefore, through an adhesion friction study, the adhesion mechanism was examined and the relationship between friction characteristics and adhesion friction on dry surfaces was derived. The wet grip characteristics of tread rubber are fully described by the hysteresis characteristics of tires, but friction characteristics on dry roads are difficult to determine without adhesion factors. The results presented herein demonstrate that the combination of hysteresis and adhesion properties in the tread rubber sufficiently explained the characteristics of the dry grip. Based on the results of this study, technologies will be developed to determine the key factors governing adhesion friction characteristics and improve dry tire braking performance.

• Journal of Adhesion and Interface
• /
• v.19 no.2
• /
• pp.84-94
• /
• 2018

Electrically debonding adhesives[EDA], one of the controlled delamination materials[CDM] is reviewed. CDM can be defined as the ability to separate adhesive bonded assemblies without causing damage to the substrates. Its application includes electronics, medical surgery, dentistry, building and general manufacturing where the opportunity to separate assemblies is important. There are several important mechanisms of EDAs; faradaic reaction, phase separation and anode detachment, cathodic debonding, gas emission mechanism, and mechanical stresses. These mechanisms are reviewed with various research results. Since the mechanism behind the electrochemical debonding of adhesives is not well understood, this review aims to help the research scientists in the industries. Finally, new applications of EDA are introduced as new business opportunity.

• Journal of Integrative Natural Science
• /
• v.9 no.3
• /
• pp.171-176
• /
• 2016

Rap1 is a key regulator of cell adhesion and migration. Although increasing evidence indicates that the Rap1 signaling pathway is involved in the process of bone remodeling, the mechanism by which Rap1 regulates osteoblastic differentiation and cell adhesion remains unknown. Here, we investigated the morphological characteristics and osteoblastic differentiation of cells expressing constitutively activated form of Rap1A (Rap1ACA) or Rap1 GTPase activating protein Rap1GAP and found that activated Rap1 induces osteoblastic differentiation and cell adhesion as well as cell spreading. When osteoblastic differentiation was induced, Rap1ACA cells showed considerably higher levels of calcium deposits than the wild-type and Rap1GAP-overexpressing cells did. Rap1ACA cells showed increased spreading and size, as well as strong cell adhesion and significantly decreased growth rates. F-actin staining using phalloidin revealed several thin thread-like filopodia around the protrusions in Rap1ACA cells, which possibly contribute to the increased cell adhesion.

• Korean Journal of Materials Research
• /
• v.15 no.1
• /
• pp.6-13
• /
• 2005

Copper based leadframe sheets were immersed in two kinds of hot alkaline solutions to form brown-oxide or blackoxide layer on the surface. The oxide-coated leadframe sheets were molded with epoxy molding compound (EMC). After post mold curing, the oxide-coated EMC-leadframe joints were machined to form sandwiched double-cantilever beam (SDCB) specimens. The SDCB specimens were used to measure the fracture toughness of the EMC/leadframe interfaces under quasi-Mode I loading conditions. After fracture toughness testing, the fracture surface were analyzed by various equipment to investigate failure path. An adhesion model was suggested to explain the failure path formation. The adhesion model is based on the strengthening mechanism of fiber-reinforced composite. The present paper deals with the introduction of the adhesion model. The explanation of the failure path with the proposed adhesion model was introduced in the companion paper.

• Proceedings of the Korean Society For Composite Materials Conference
• /
• 1999.11a
• /
• pp.36-39
• /
• 1999

Steel tire cords were coated via RF Plasma Polymerization of acetylene in order to enhance adhesion to rubber compounds. Adhesion of tire cords was measured by TACT as a function of plasma polymerization and argon etching conditions such as power, treatment time and chamber pressure. Tested tire cords were analysed by SEM to elucidate the adhesion mechanism. The highest adhesion values were obtained with argon etching condition at 90W, 10min, 30mtorr followed by acetylene plasma polymerization condition at 10W, 30sec., 30mtorr. In SEM analysis, the plasma polymerized tire cord at the optimized condition showed 100% rubber coverage as observed from brass-plated steel tire cords.

• Molecules and Cells
• /
• v.38 no.9
• /
• pp.821-828
• /
• 2015

Monocytes are the major inflammatory cells that infiltrate most solid tumors in humans. The interaction of tumor cells with infiltrating monocytes and their adhesion to these monocytes play a significant role in altering the tumor to become more aggressive. Recently, exposure to lipopolysaccharide (LPS) was suggested to promote cancer cell adhesion to monocytes; however, little is known about the details of the signaling mechanism involved in this process. In this study, we found that LPS up-regulates ICAM-1 expression in MDA-MB-231 breast cancer cells, which facilitates their adhesion to THP-1 monocytes. In addition, we analyzed the signaling mechanism underlying the up-regulation of ICAM-1 and found that the siRNA-mediated depletion of BLT2 markedly suppressed the LPS-induced expression of ICAM-1 in MDA-MB-231 cells and the subsequent adhesion of these cells to THP-1 monocytes. Moreover, we demonstrated that myeloid differentiation primary response gene 88 (MyD88) lies downstream of LPS/TLR4 and upstream of BLT2 and that this 'MyD88-BLT2' cascade mediates ERK activation and subsequent ICAM-1 expression, which is critical for the adhesion of MDA-MB-231 cells to THP-1 monocytes. Taken together, our results demonstrate for the first time that LPS up-regulates ICAM-1 expression in breast cancer cells via a MyD88-BLT2-ERK-linked signaling cascade, leading to the increased adhesion of breast cancer cells to monocytes.