• 제목/요약/키워드: Pd activator

검색결과 16건 처리시간 0.023초

Novel Environmentally Benign and Low-Cost Pd-free Electroless Plating Method Using Ag Nanosol as an Activator

  • Kim, Jun Hong;Oh, Joo Young;Song, Shin Ae;Kim, Kiyoung;Lim, Sung Nam
    • Journal of Electrochemical Science and Technology
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    • 제8권3호
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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.

Pd활성제와 열처리 온도에 의한 ${SnO_2}/{Al_2}{O_3}$ 가스센서에 미치는 감응효과 (The effect of Pd activator and annealing temperatures on the response characteristecs of the ${SnO_2}/{Al_2}{O_3}$gas sensor)

  • 전춘생
    • 한국재료학회지
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    • 제4권3호
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    • pp.295-300
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    • 1994
  • 이 논문은 $SnO_2$에 소량의 Pd를 첨가하여 이것을 $Al_2O_3$기판위에 진공증착시켜 가스소자를 제작한 후, 소자의 감지특성에 영향을 미치는 열처리 온도, 소자의 온도, Pd의 첨가량의 변화 효과를 조사한 것이다. 소자의 열처리 온도가 $550^{\circ}C$일때와 소자의 동작온도가 $350^{\circ}C$일때 ethanol gas에 접촉시 소자 저항이 가장 낮았다. Pd 1 wt%를 첨가한 경우 에탄올 가스에 대한 소자의 감지특성이 가장 양호하였으며, 저농도 영역에서 특히 우수하였다.

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포도당 환원제와 PdCl2 촉매를 사용한 무전해 은도금 PET 직물의 제조 (Preparation of Electromagnetic Wave Shielding Fabrics by Electroless Silver Plating using PdCl2 and Dextrose)

  • 김수미;송화순
    • 한국의류학회지
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    • 제32권2호
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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.

무전해 니켈·팔라듐·금도금 표면처리 공정의 도금 번짐 불량 및 개선 (Prevention of Running Blots between the Patterns during the Electroless Nickel Electroless Palladium Immersion Gold (ENEPIG) Surface Finish)

  • 엄기헌;서정욱;원용선
    • 청정기술
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    • 제19권2호
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    • pp.84-89
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    • 2013
  • 무전해 니켈 팔라듐 금 표면처리 공정의 도금 번짐 불량의 근본적인 원인을 이해하고 이를 해결하기 위한 방법을 제시하였다. 이에 계산화학을 이용하여 공정을 정성적으로 설명하고 이를 바탕으로 가정을 검증하기 위한 실험을 계획하였다. 도금 번짐으로 발전되는 고분자 레진 위의 팔라듐 시드의 핵 생성을 막는 것에 초점을 맞추어 고분자 레진과 화학적으로 결합력이 약한 $PdCl_2$ 팔라듐 촉매를 도입하였으며 이 촉매가 수용액 중에서 추가적인 가수분해 반응으로 더 안정한 $Pd(OH)_2$를 형성함으로써 고분자 레진 위에 팔라듐 시드의 원천으로 작용하지 않도록 염산(HCl)의 농도를 높이거나 팔라듐 활성화 공정의 온도를 낮추어 보았다. 계산화학은 매 단계 실험의 이론적인 근거를 제시해 주었으며 실험 결과를 해석하는 데 큰 도움을 주었다. 이와 같이 실험과 이론을 접목시킨 본 연구의 접근법은 관련 공정에서 매우 유용하게 활용될 수 있을 것으로 기대된다.

Root Resorption in Streptozotocin-induced Diabetic Rats with Ligature-induced Periodontitis

  • Kim, Ji-Hye;Lee, Dong-Eun;Park, Jung-Chul;Kim, Yoon Jae;Cha, Jeong-Heon;Bak, Eun-Jung;Yoo, Yun-Jung
    • International Journal of Oral Biology
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    • 제40권3호
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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.

Smooth muscle cell 증식에 있어 NF-κ ligand의 receptor activator의 역할 (The Role of Receptor Activator of NF-κ Ligand in Smooth Muscle Cell Proliferation)

  • 김현주
    • 생명과학회지
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    • 제16권6호
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    • pp.1066-1070
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    • 2006
  • Smooth muscle cell (SMC)의 증식은 혈관성장에 의한 질환의 발병기전의 중요한 요소이다. 혈관 손상 후 SMC의 성장조절에 대한 분자적 기작에 대한 연구는 치료제 개발에 있어 중요한 의미를 지닌다. 이에, 본 연구에서는 TNF family인 RANKL가 SMC의 증식을 촉진함을 입증하였다. RANKL는 p21의 발현을 감소시키고 p21의 promoter활성을 저해함으로써 SMC의 성장을 증가시켰다. 또한 ERK와 p38 MAPK의 활성이 RANKL에 의해 증가하였으며, ERK/p38의 저해제는 RANKL에 의해 유도되는 SMC의 성장을 완전히 억제하였다. 이러한 결과는 ERK와 p38 MAPK가 RANKL에 의해 유도되는 SMC의 증식에 중요한 역할을 함을 보여주는 것이다. 즉, RANK-RANKL-ERK/p38이 SMC의 증식을 매개하는 중요 분자이며, 이들 분자는 혈관 질환을 막는 새로운 치료제 개발의 표적분자가 될 수 있음이 입증되었다.

Steric and Electronic Effects of Tetradentate Nickel(II) and Palladium(II) Complexes toward the Vinyl Polymerization of Norbornene

  • Lee, Dong-Hwan;Lee, Jung-Hwan;Eom, Geun-Hee;Koo, Hyo-Geun;Kim, Cheal;Lee, Ik-Mo
    • Bulletin of the Korean Chemical Society
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    • 제32권6호
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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.

인간 유방 MCF-12A 세포에서 PI3-kinase 경로를 통한 BCAR3의 estrogen response element 활성화 (BCAR3 Activates the Estrogen Response Element through the PI3-kinase/Akt Pathway in Human Breast MCF-12A Cells)

  • 오명주;하주연;전병학
    • 생명과학회지
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    • 제32권11호
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    • pp.882-889
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    • 2022
  • Breast cancer anti-estrogen resistance 3 (BCAR3)는 유방암에서 항에스트로겐 내성을 유도하는 유전자들 중의 하나로 발견되었다. 우리는 이미 BCAR3가 c-jun, activator protein-1, serum response element의 promoter 등을 활성화하는 것을 보고하였다. 본 연구에서 우리는 정상 유방세포인 MCF-12A에서 estrogen response element (ERE) 활성에서의 BCAR3의 기능을 조사하였다. BCAR3의 발현이 ERE를 활성화하는 것을 발견하였다. 이 ERE 활성화는 17β-estradiol에 의해 더욱 증가하였고, 이는 항에스트론겐인 tamoxifen에 의해 억제되지 않았다. 다음으로 우리는 ERE 활성화를 이끄는 BCAR3의 신호전달 경로를 연구하였다. BCAR3에 의한 ERE 활성화는 phosphatidylinositol (PI) 3-kinase 경로 억제제인 LY294002와 AZD5363에 의해서는 억제되었으나, Mitogen-activated protein kinase 경로 억제제인 PD98059와 U0126에 의해서는 억제되지 않았다. ERE 활성화는 PI3-kinase의 catalytic subunit p110α와 Akt의 active mutant에 의해서는 유도되었고, 이 활성화는 추가적인 BCAR3에 의해서는 더욱 증가하지 않았다. 이러한 결과로부터 우리는 BCAR3가 PI3-kinase/Akt 신호전달경로를 통하여 ERE 활성화에 중요한 역할을 하는 것을 제시한다.

Toxoplasma gondii IST suppresses inflammatory and apoptotic responses by inhibiting STAT1-mediated signaling in IFN-γ/TNF-α-stimulated hepatocytes

  • Seung-Hwan Seo;Ji-Eun Lee;Do-Won Ham;Eun-Hee Shin
    • Parasites, Hosts and Diseases
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    • 제62권1호
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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.

A Novel All-trans Retinoid Acid Derivative N-(3-trifluoromethyl-phenyl)-Retinamide Inhibits Lung Adenocarcinoma A549 Cell Migration through Down-regulating Expression of Myosin Light Chain Kinase

  • Fan, Ting-Ting;Cheng, Ying;Wang, Yin-Feng;Gui, Shu-Yu;Chen, Fei-Hu;Zhou, Qing;Wang, Yuan
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권18호
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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.