• Physical Therapy Korea
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• v.20 no.3
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• pp.27-35
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• 2013

The aim of this study was to compare the electromyographic (EMG) activity levels of the scapular upward rotators [upper trapezius (UT), lower trapezius (LT), and serratus anterior (SA)] and other scapular muscles [posterior deltoid (PD), levator scapulae (LS), and infraspinatus (IS)] during isometric lower trapezius exercises. Twenty males with no medical history of shoulder pain or upper extremity disorders were recruited for this study. EMG activity was recorded from the UT, LT, SA, PD, LS, and IS while subjects performed three different exercises: Prone arm lift (PAL), Backward rocking diagonal arm lift (BRDAL), Modified Prone Cobra (MPC). One-way analysis of variance (ANOVA) was used to determine any significant differences among the three exercises. A lower relative activation of UT, LT, and SA was seen with the MPC than with the other exercises (p<.05). The relatively lower activation of the UT identified, the MPC exercise as the preferred choice for preferential strengthening the LT (p<.05). However, a higher activation in the PD, LS, and IS occurred with the MPC than with the other exercises (p>.05). The recruitment pattern of synergist varied depending on the exercise posture. These findings suggest that exercise posture is an important factor in the selection of strengthening exercise for weak muscle.

• Textile Coloration and Finishing
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• v.22 no.1
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• pp.77-82
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• 2010

Highly conductive yarn was successfully obtained using electroless nickel plating method with palladium activation. In the presence of palladium seed on surface of fibers as a catalyst, continuos nickel layer produced on surface of fibers by reducing $Ni${2+}$ ion in the electroless plating bath to $Ni^0$. It was found that the Pd-activation using $SnCl_2$ and $PdCl_2$ to deposit palladium seeds on the surface of fibers plays a key role in the subsequent electroless plating of nickel. It also found that electroless nickel plating on the fibers can induce the nickel-plated $ELEX^{(R)}$ fibers to improve the electrical conductivity of the fibers. The thickness of nickel coating layer on the Pd-activated $ELEX^{(R)}$ fibers and specific conductivity of the fiber were increased through electroless plating time. The temperature of nickel plating bath was very effective to enhance the nickel deposition rate.

• Transactions of the Korean hydrogen and new energy society
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• v.9 no.1
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• pp.25-30
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• 1998

4-probe resistivity measurement technique was used to study kinetics of hydrogen absorption on Pd film ($180{\AA}$ thick) in the ${\alpha}$ phase. Hydrogen gas was introduced to the activated Pd film. For very low hydrogen concentration the following rate law is valid in ${\alpha}$ phase very thin Pd film $$v=k\frac{1}{1+KX{_H}}PH{_2}-k^{\prime}\frac{KX{_H}{^2}}{1+KX{_H}}$$ which is similar to that of bulk. The activation energy of the forward reaction is 4.6kcal/mol H and of the backward reaction 8.4kcal/mol H, which yields the reaction enthalpy -3.8kcal/mol H in the temperature range between 25 and $40^{\circ}C$. The values of activation and enthalpy of thin film are rather smaller than that of bulk sample. This may be due to surface area difference between bulk and film.

• Korean Journal of Clinical Laboratory Science
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• v.42 no.1
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• pp.46-54
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• 2010

Ceramide induces cell death in a variety of cell types however, the underlying molecular mechanisms related to renal epithelial cells remain unclear. The present study was undertaken to determine the role of extracellular signal-regulated protein kinase (ERK) in ceramide-induced cell death in renal epithelial cells. An established renal proximal tubular cell line of opossum kidney (OK) cells was used for this research. Ceramide induced apoptotic cell death in these cells. Western blot analysis showed that ceramide induced activation of ERK. The ERK activation and cell death induced by ceramide were prevented by the ERK inhibitor PD98059. Ceramide caused cytochrome C release from mitochondria into the cytosol as well as activation of caspase-3. Both effects were prevented by PD98059. The ceramide-induced cell death was also prevented by a caspase inhibitor. These results suggest that ceramide induces cell death through an ERK-dependent mitochondrial apoptotic pathway in OK cells.

• Proceedings of the Korean Institute of Surface Engineering Conference
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• 2015.05a
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• pp.181-182
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• 2015

본 실험에서는 PET 위 무전해 도금을 위한 대안 공정 개발을 목적으로 은(Ag)와 과망간산염($MnO_4{^-}$)를 사용하여 기존에 일반적으로 사용된 Sn/Pd의 Sensitization과 Activation process를 대체하는 기술을 연구했다. Palladium(Pd)의 경우 공정비용에서 높은 부분을 차지하기 때문에 이를 대신하여 Ag를 사용했으며, PET 표면의 전처리를 위해 Ultra Violet과 과망간 산염을 이용하여 표면의 친수성을 높였다. 과망간산염을 사용하여 표면을 전처리하는 과정에서 이산화망간($MnO_2$)과 알코올 작용기가 생성되는데 Ag activation 단계에서 촉매 생성에 중간 매개체 역할을 하는 것으로 사료된다. 이와 같은 결론을 도출 하기 위해서 표면 위 Ag의 화학적 구조 및 상 분석을 위해 XPS와 TEM이 사용되었으며 표면에서 Ag는 Ag-O와 같은 Silver oxide의 형태와 Ag-Mn-O와 같은 Compound로 무전해 도금을 위한 촉매 역할 하는 것으로 판단된다.

• Journal of radiological science and technology
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• v.21 no.1
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• pp.59-64
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• 1998

[ $CaSO_4$ ] thermoluminescent phosphors was made by sintring the $CaSO_4$ after doping the transition elements Tm, Pd, Dy, V, Mo, Zr. The maximum Peaks are found in the measured $CaSO_4$(Tm, Pd, Dy, V, Mo, Zr) TL glow curve at $130^{\circ}C,\;110^{\circ}C,\;140^{\circ}C,\;100^{\circ}C$, and $120^{\circ}C$ when the heating rate is $5^{\circ}C/sec$. The activation energy of the main peak has been estimated by the peak shape method. The estimated activation energies are 1.02eV, 1.32eV, 1.12eV, 0.80eV, and 1.17eV, respectively. The thermoluminescence process in $CaSO_4$(Tm, Pd, Dy, V, Mo, Zr)are found to the 2nd order when the main peak of the glow curve is analyzed by peak shape method. The dose responses of $CaSO_4$(Tm, Pd, Dy, V, Mo, Zr) phosphors are linear within $4{\times}10^{-4}{\sim}1Gy$ of X-rays.

• Journal of Environmental Science International
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• v.31 no.5
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• pp.423-429
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• 2022

Parkinson's Disease (PD) is a chronic neurodegenerative disorder caused by the progressive loss of dopaminergic neurons, leading to decreased dopamine levels in the midbrain. Although the specific etiology of PD is not yet known, oxidative stress, inflammation, and subsequent apoptosis have been proposed to be closely related to PD pathophysiology. Cera Flava (CF) is a natural extract obtained from beehives and is isolated through the heating, compression, filtration, and purification of beehives. CF has been used in traditional medicines for its various clinical and pharmacological effects. However, its effects on neurodegenerative diseases are unknown. Therefore, we investigated the effects of CF against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD in mice and explored the underlying mechanism of action. In MPTP-induced PC12 cells, CF protected NADH dehydrogenase activity and inhibited lactate dehydrogenase. In the mouse model, CF promoted recovery from movement impairments, prevented dopamine depletion, and protected against MPTP-induced dopaminergic neuronal degradation. Moreover, CF downregulated glial and microglial activation. Taken together, our results suggest that CF improves behavioral impairments and protects against dopamine depletion in MPTP-induced toxicity by inhibiting glial and microglial activation.

• Bulletin of the Korean Chemical Society
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• v.28 no.12
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• pp.2369-2376
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• 2007

N2O has been found from experimental and theoretical considerations to bind on-top to the Pd(110) surface in a tilted end-on fashion via its terminal N atom. We use a frontier orbital description of the bonding interactions in the Pd-N2O system to obtain molecular insight into the catalytic mechanism of the activation of N2O by the Pd(110) surface giving rise to the formation of N2 and O on the surface. For the tilted end-on N2O binding mode, the LUMO 3π of N2O has good overlap with the Pd dσ and dπ orbitals which can serve as the electron donors. The donor-acceptor orbital overlap is favorable for electron transfer from Pd to N2O and is expected to dominate the surface reaction pathway of N2O decomposition.

• Journal of Ginseng Research
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• v.22 no.3
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• pp.200-205
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• 1998

Isolated rabbit jejunal segments were used to study the effects of ginseng total saponins (GTS) , protopanaxatriol saponins (PT) and protopanaxadiol saponins (PD) on intestinal contractility. GTS, PT and PD caused a dose-dependent decrease in intestinal spontaneous movements, and PT was the most efficacious of them. The effect of GTS, PT and PD were not blocked by pretreatment with phentolamine (10-6 M), yohimbine (10-6 M), d1-propranolol (10-6 M), naloxone(10-6∼10-5M), Nu-nitro-L-arginine methyl ester (10-4 M), methylene blue (10-5M), and N-ethylmaleimide (10-4 M). However, pretreatment with tetraethylammonium chloride (3-10 mM) antagonized the effect of GTS, PT and PD. Furthermore, 4-amlnopyridine (1 mM) also inhibited the effect of GTS, PT and PD. The results suggest that GTS, PT and PD inhibited the spontaneous movements in isolated rebait jejunum by causing hyperpolarization through an activation of K+ channels directly.

• Molecular & Cellular Toxicology
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• v.4 no.2
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• pp.106-112
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• 2008

Parkinson's disease (PD) progresses severely by a gradual loss of dopaminergic neurons in the substantia nigra (SN). Epidemiological studies showed that the incidences of PD were reduced by smoking of which the major component, nicotine might be neuroprotective. But the function of nicotine, which might suppress the incidences of PD, is still unknown. Fortunately, recently it was reported that a glial reaction and inflammatory processes might participate in a selective loss of dopaminergic neurons in the SN. The levels of tumour necrosis factor (TNF)-${\alpha}$ synthesised by astrocytes and microglia are elevated in striatum and cerebrospinal fluid (CSF) in PD. TNF-${\alpha}$ kills the cultured dopaminergic neurons through the apoptosis mechanism. TNF-${\alpha}$ release from glial cells may mediate progression of nigral degeneration in PD. Nicotine pretreatment considerably decreases microglial activation with significant reduction of TNF-${\alpha}$ mRNA expression and TNF-${\alpha}$ release induced by lipopholysaccharide (LPS) stimulation. Thus, this study was intended to explore the role of nicotine pretreatment to inhibit the expressions of TNF-${\alpha}$ mRNA in human fetal astrocytes (HFA) stimulated with IL-$1{\beta}$. The results are as follows: HFA were pretreated with 0.1, 1, and $10{\mu}g/mL$ of nicotine and then stimulated with IL-$1{\beta}$ (100 pg/mL) for 2h. The inhibitory effect of nicotine on expressions of TNF-${\alpha}$ mRNA in HFA with pretreated $0.1{\mu}g/mL$ of nicotine was first noted at 8hr, and the inhibitory effect was maximal at 12 h. The inhibitory effect at $1{\mu}g/mL$ of nicotine was inhibited maximal at 24 h. Cytotoxic effects of nicotine were noted above $10{\mu}g/mL$ of nicotine. Moreover, Nicotine at 0.1, 1 and $10{\mu}g/mL$concentrations significantly inhibited IL-$1{\beta}$-induced TF-${\kappa}B$ activation. Collectively, these results indicate that in activated HFA, nicotine may inhibit the expression of TNF-${\alpha}$ mRNA through the pathway which suppresses the NF-${\kappa}B$ activation. This study suggests that nicotine might be neuroprotective to dopaminergic neurons in the SN and reduce the incidences of PD.