• Journal of Electrochemical Science and Technology
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• v.8 no.3
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• pp.215-221
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• 2017

The electroless plating process largely consists of substrate cleaning, seed formation (activator formation), and electroless plating. The most widely used activator in the seed formation step is Pd, and Sn ions are used to facilitate the formation of this Pd seed layer. This is problematic because the Sn ions interfere with the reduction of Cu ions during electroless plating; thus, the Sn ions must be removed by a hydrochloric acid cleaning process. This method is also expensive due to the use of Pd. In this study, Cu electroless plating was performed by forming a seed layer using a silver nanosol instead of Pd and Sn. The effects of the Ag nanosol concentration in the pretreatment solution and the pretreatment time on the thickness and surface morphology of the Cu layer were investigated. The degrees of adhesion to the substrate were similar for the electroless-plated Cu layers formed by conventional Pd activation and those formed by the Ag nanosol.

• Korean Journal of Materials Research
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• v.4 no.3
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• pp.295-300
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• 1994

This paper is aimed to study the effect of Pd activator, the annealing temperature, and operating temperatures on the response characteristics of the $SnO_2/Al_2O_3$ sensor. The resistance of device has shown minimum value when annealing temperature and operating temperature of device are $550^{\circ}C$ and $350^{\circ}C$ respectively in ethanol gas. And the response characteristics of the device showed the best results when lwt% Pd was added to SnOz especially in low concentration of ethanol gas.

• Journal of the Korean Society of Clothing and Textiles
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• v.32 no.2
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• pp.319-327
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• 2008

The purpose of this study is to propose the development of high quality electromagnetic wave shielding fabrics. Silver nitrate is used for polyester fabric as an electromagnetic wave shielding material. The effects of activators and electroless silver plating condition on the evenness and adhesion of silver to fabrics, are observed through the SEM micrographs. Surface morphology and wash-ability are measured using SEM. The results are as follows: The optimum weight loss by alkaline hydrolysis of polyester fabrics is about 20%. The optimum concentration of $SnCl_2$ and $PdCl_2$in catalyst reaction using $PdCl_2$ as an activator is 2.5g/L and 0.5g/L, respectively. The optimum concentration of dextrose to improve adhesion between the silver plating and fabrics is 45g/L. The optimum concentration of silver nitrate in the catalyst reaction, using $PdCl_2$ as an activator is 56g/L, respectively. The optimum plating temperature and time are $15^{\circ}C$ and 30minutes, respectively.

• Clean Technology
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• v.19 no.2
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• pp.84-89
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• 2013

The running blots between patterns during electroless nickel electroless palladium immersion gold (ENEPIG) surface finish of printed circuit board (PCB) are investigated and a proper solution is presented. Computational chemistry is first employed to understand the process and experiments are then designed to verify the proposed ideas. A $PdCl_2$ activator which has relatively weak chemical bonding to the epoxy resin is introduced to prevent the formation of palladium seeds on the epoxy resin and a couple of operational measures such as increasing HCl concentration and lowering the temperature of Pd activation process are executed to prevent a further hydrolysis of $PdCl_2$ to more stable $Pd(OH)_2$ in aqueous solution. Computational chemistry provides thermodynamic backgrounds for experiments and their results. This combined approach is expected to be very useful in the research of relevant processes.

• International Journal of Oral Biology
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• v.40 no.3
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• pp.111-116
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• 2015

To determine the effect of diabetes on root resorption in periodontitis, we investigated odontoclast formation and root resorption in diabetic rats with periodontitis. Odontoclast formation was observed in three groups of F344 rats: Controls (C) were normal rats without diabetes or periodontitis; the periodontitis (P) group had mandibular first molars to be ligatured; the periodontitis with diabetes (PD) group was intravenously administered streptozotocin (50 mg/kg) to induce diabetes and had mandibular first molars to be ligatured. On days 3, 10, and 20 after ligature, tumor necrosis factor (TNF)-${\alpha}$ and receptor activator of nuclear factor-${\kappa}B$ ligand (RANKL) expression, odontoclast formation, and root resorption areas were evaluated by immunohistochemistry, tartrate-resistant acid phosphatase staining, and hematoxylin and eosin staining, respectively. The PD group showed frequent urination, weight loss, and hyperglycemia. Numbers of TNF-${\alpha}$- and RANKL-positive cells were higher in the P and PD groups than in the C group. It was more prevalent in PD group on day 3. Odontoclast formation was greater in the P and PD groups than in the C group on days 3 and 10, then decreased to same level as the C group by day 20. Root resorption in the PD and P groups showed increases on days 3 and 10, respectively, compared to the C group. These results suggest that diabetes may transiently increase root resorption on day 3 with high expression of TNF-${\alpha}$ and RANKL after periodontitis induction. This study could aid the understanding of root resorption in diabetic patients with periodontitis.

• Journal of Life Science
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• v.16 no.6
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• pp.1066-1070
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• 2006

Smooth muscle cell (SMC) proliferation is important in the pathogenesis of vascular proliferative disorders. Understanding of the molecular mechanism underlying SMC growth after arterial injury would have therapeutic implications. Here we report that receptor activator of $NF-{\kappa}B$ ligand (RANKL), a member of tumor necrosis factor (TNF) family, promotes the proliferation of SMC, leading to decreased expression of p21 and enhancement of SMC growth. ERK and p38 phosphorylation was enhanced after RANKL treatment in SMC. Inhibition of ERK/p38 MAPK activity by PD98059/SB203580 completely abolished RANKL-induced proliferation of SMC, indicating ERK and p38 MAPK are essential for RANKL-induced SMC proliferation. Taken together, our findings demonstrate that RANK-RANKL-ERK/p38 pathway is important for proliferation of SMC and that these molecules may be the new therapeutic targets for the prevention of vascular diseases.

• Bulletin of the Korean Chemical Society
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• v.32 no.6
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• pp.1884-1890
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• 2011

A series of Ni(II) and Pd(II) complexes bearing N4-type tetradentate ligands, [Ni($X^1X^2$-6-$Me_2bpb$) 1] and [Pd($X^1X^2$-6-$Me_2bpb$) 2]; 6-$Me_2bpb$ = N,N'-(o-phenylene)bis(6-methylpyridine-2-carboxamidate), $X^1$ = Cl, H, or $CH_3$, $X^2$ = $NO_2$, Cl, F, H, $CH_3$, or $OCH_3$) were designed, synthesized, and characterized to investigate electronic and steric effects of ligand on the norbornene polymerization catalysts. Using modified methylaluminoxanes as an activator, the complexes exhibited high catalytic activities for the polymerization of norbornene and the nickel complexes exhibited better catalytic activity the palladium complexes. Ni complex 1a with $NO_2$ group on the benzene ring showed the highest catalytic activity of $4.9{\times}10^6$ g of PNBEs/$mol_{Ni}{\cdot}h$ and molecular weight of $15.28{\times}10^5$ g/mol with PDI < 2.30. Complexes with electron-withdrawing groups are more thermally stable (> 100 $^{\circ}C$), and tend to afford higher polymerization productivities than the ones having electron-donating groups. Amorphous polynorbornenes were obtained with good solubility in halogenated aromatic solvents. A vinyl addition mechanism has been proposed for the catalytic polymerization.

• Journal of Life Science
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• v.32 no.11
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• pp.882-889
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• 2022

Breast cancer anti-estrogen resistance 3 (BCAR3) has been identified as one of the genes that induces anti-estrogen resistance in breast cancer. We have previously reported that BCAR3 activates promoters of c-Jun, activator protein-1, and the serum response element. In this study, we investigated the functional role of BCAR3 in the activation of the estrogen response element (ERE) in normal human breast MCF-12A cells. Transient expression of BCAR3 induced ERE activation, which was further increased by 17β-estradiol treatment but was not blocked by the anti-estrogen tamoxifen. Next, we studied the signaling pathway of BCAR3 leading to ERE activation. BCAR3-mediated ERE activation was inhibited by LY294002 and AZD5363, inhibitors of the phosphatidylinositol (PI) 3-kinase pathway, but not by PD98059 and U0126, inhibitors of the mitogen-activated protein kinase pathway. ERE activation was induced by the catalytic subunit p110α. of PI3-kinase or the active mutant of Akt, and this activation was not further increased by additional BCAR3 transfection. Based on these results, we propose that BCAR3 plays an important role in ERE activation through the PI3-kinase/Akt pathway in human breast MCF-12A cells.

• Parasites, Hosts and Diseases
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• v.62 no.1
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• pp.30-41
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• 2024

The dense granule protein of Toxoplasma gondii, inhibitor of signal transducer and activator of transcription 1 (IST) is an inhibitor of signal transducer and activator of transcription 1 (STAT1) transcriptional activity that binds to STAT1 and regulates the expression of inflammatory molecules in host cells. A sterile inflammatory liver injury in pathological acute liver failures occurs when excessive innate immune function, such as the massive release of IFN-γ and TNF-α, is activated without infection. In relation to inflammatory liver injury, we hypothesized that Toxoplasma gondii inhibitor of STAT1 transcription (TgIST) can inhibit the inflammatory response induced by activating the STAT1/IRF-1 mechanism in liver inflammation. This study used IFN-γ and TNF-α as inflammatory inducers at the cellular level of murine hepatocytes (Hepa-1c1c7) to determine whether TgIST inhibits the STAT1/IRF-1 axis. In stable cells transfected with TgIST, STAT1 expression decreased with a decrease in interferon regulatory factor (IRF)-1 levels. Furthermore, STAT1 inhibition of TgIST resulted in lower levels of NF-κB and COX2, as well as significantly lower levels of class II transactivator (CIITA), iNOS, and chemokines (CLXCL9/10/11). TgIST also significantly reduced the expression of hepatocyte proapoptotic markers (Caspase3/8/9, P53, and BAX), which are linked to sterile inflammatory liver injury. TgIST also reduced the expression of adhesion (ICAM-1 and VCAM-1) and infiltration markers of programmed death-ligand 1 (PD-L1) induced by hepatocyte and tissue damage. TgIST restored the cell apoptosis induced by IFN-γ/TNF-α stimulation. These results suggest that TgIST can inhibit STAT1-mediated inflammatory and apoptotic responses in hepatocytes stimulated with proinflammatory cytokines.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.18
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• pp.7687-7692
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• 2014

Aim: To observe the effects of a novel all-trans retinoid acid (ATRA) derivative, N-(3-trifluoromethyl-phenyl)-retinamide (ATPR), on lung adenocarcinoma A549 cells and to explore the potential mechanism of ATPR inhibiting of A549 cell migration. Materials and Methods: The cytotoxicity of ATRA and ATPR on A549 cells was assessed using MTT assay. Wound healing assays were used to analyze the influences of ATRA, ATPR, ML-7 (a highly selective inhibitor of myosin light chain kinase (MLCK)), PMA (an activator of MAPKs) and PD98059 (a selective inhibitor of ERK1/2) on the migration of A549 cells. Expression of MLCK and phosphorylation of myosin light chain (MLC) were assessed by Western blotting. Results: ATRA and ATPR inhibited the proliferation of A549 cells in a dose- and time-dependent manner, and the effect of ATPR was much more remarkable compared with ATRA. Relative migration rate and migration distance of A549 cells both decreased significantly after treatment with ATPR or ML-7. The effect on cell migration of PD98059 combining ATPR treatment was more notable than that of ATPR alone. Moreover, compared with control groups, the expression levels of MLCK and phosphorylated MLC in A549 cells were both clearly reduced in ATRA and ATPR groups. Conclusions: ATPR could suppress the migration and invasion of A549 cells, and the mechanism might be concerned with down-regulating the expression of MLCK in the ERK-MAPK signaling pathway, pointing to therapeutic prospects in lung cancer.