• YAKHAK HOEJI
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• v.47 no.1
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• pp.31-36
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• 2003

To investigate the effect of protein kinase on melanin production via cAMP-dependent pathway, we measured the melanin amount and tyrosinase activity in B16 melanoma cells stimulated by alpha-melanocyte stimulating hormone (MSH), forskolin and 8-Br-cAMP. MSH, forskolin and 8-Br-cAMP significantly increased both melanin production and tyrosinase activity in B16 cells. Melanin production and tyrosinase activity by MSH are significantly inhibited by cyclic AMP-dependent protein kinase inhibitor (KT5720) and protein kinase C down-regulation treated with PMA. Bisindolmaleimide (1$\mu$M), protein kinase C inhibitor, significantly inhibited melanin production and tyrosinase activity stimulated by MSH, forskolin and 8-Br-cAMP with the following order of potency: MSH＞forskolin＞8-Br-cAMP. Tyrosine kinase inhibitor, genistein and DHC, significantly inhibited both, but the inhibitory effect was more potent in 8-Br-cAMP-stimulated B16 cells than MSH-stimulated cells. NFkB inhibitor (parthenolide) significantly inhibited melanin production and tyrosinase activity. Neither melanin production nor tyrosinase activity induced by MSH, forskolin and 8-Br-cAMP were affected by KN-62 (calmodulin-dependent protein kinase II inhibitor), PD098059 (mitogen-activated protein kinase inhibitor, MAPKK) and worthmannin (phosphatidylinositol 3-kinase inhibitor). These results suggest that both protein kinase C and tyrosine kinase are involved in melanin production by cyclic AMP-dependent pathway and NFkB pathway may play an important role in cyclic AMP-dependent melanin production in B16 melanoma cells.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.11 no.1
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• pp.39-48
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• 1978

1) The decrease in strength of Raschel twines at Raschel joints is regarded to be due mainly to the frictional force between yarns and the unbalanced tensile distribution by the deformation of the joints. The rate of the decrease is about $13\%$ in lengthwise pull and 22 to $26\%$ in breadthwise pull. 2) The 3-course joint is less in deformation and stronger than the 2-course joint in all cases of pulls. 3) The variation of Raschel joint strength $T_R$ with the angle $\varphi$ between the adjacent bars is expressed as $T_R=T_{R0}-k\varphi$ where $T_{R0}$ is the strength at $\varphi=0^{\circ}$ and K is a constant. 4) The tensile strength ${\sigma}R$ and tile breaking energy $E_R$ of Raschel netting are given by $${\sigma}R=KN\;or\;${\sigma}R=T_RN$$ and $$E_R=AN$$ respectively, where N is the number of meshes at the pulling side, and K and A are constants. But the breaking energy of the netting is almost constant independent of tile variation of N. 5) The Raschel netting with some bars cut already breaks from tile joints of the bars next to the cut bars and its tensile strength, breaking energy, and breaking elongation decrease largily even if only one bar is in already cut state. 6) The tearing strength of Raschel netting is almost equal to the tensile strength of its single joint pulled by two bars. 7) The twisted joint is much more excellent in strength than the knot or the Raschel joint. The knot strength is 69 to $76\%$, and the Raschel joint strength is 71 to $74\%$ in lengthwise pull and 62 to $67\%$ in breadthwise pull, respectively, of the twisted joint strength.

• Korean Journal of Remote Sensing
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• v.30 no.5
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• pp.677-686
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• 2014

Sea ice covers wide area in Terra Nova Bay in East Antarctica where the Jangbogo Antarctic Research Station was built in 2014, which affects greatly on the sailing of an icebreaker research vessel. In this study, we analyzed the optimum sea route and sailable period of the icebreaker to visit the Jangbogo Antarctic Research Station by using sea ice concentration data observed by passive microwave sensors such as Special Sensor Microwave/Imager (SSM/I) and Special Sensor Microwave Imager/Sounder (SSMIS) for the last decade, and by using sea route of the Araon, an icebreaker of Republic of Korea, from 2010 to 2012. It is found that Araon sailed in the route of sea ice concentration up to 78%. Sailing speed of the Araon decreased due to increasing sea ice concentration. However, Araon maintained the speed close to the average speed for the entire sailing period (~11 kn) in the route of sea ice concentration up to 70%. Therefore, we confirm that the Araon can sail typically in the route which shows sea ice concentration below 70%. We derived annually available sailing period in recent 10 years for the sea route of the Araon in 2010, 2011 and 2012, which is defined as the period showing sea ice concentration below 70% through the route. Maximum sailable period was analyzed to be 61 and 62 days for the route of the Araon in 2010 and 2011, respectively. However, the typical sailing in the routes was unavailable in some years because sea ice concentration was higher than 70% through the routes. Meanwhile, the sailable period for the routes of the Araon in 2012 was observed in every year, which was a minimum of 15 days and is a maximum of 89 days. Therefore, we could suggest that optimum route of icebreaker to visit the Jangbogo Antarctic Research Station is the route of the Araon in 2012. High resolution images from SAR or optical sensors are necessary to investigate sea ice condition near shoreline of Jangbogo research station due to several kilometers of low resolution of sea ice concentration.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.425-434
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• 1997

Many reports represent that angiotensin II (ANG II) caused a dose dependent biphasic effects on fluid transport in the proximal tubule. However, respective roles of different signaling pathways in mediating these effects remain unsettled. The aim of the present study was to examine signaling pathways at high doses of ANG II on the $Na^+$ uptake of primary cultured rabbit renal proximal tubule cells(PTCs) in hormonally defined serum-free medium. High concentrations of ANG II $(>10^{-9}\;M)$ inhibited $Na^+$ uptake and increased $[Ca^{2+}]_i\;level$ in the PTCs. However, low concentrations of $(<10^{-11}\;ANG\;II)$ stimulated $Na^+$ uptake and did not affect $[Ca^{2+}]_i\;level$. 8-(N, N-diethylamino)-octyl-3,3,5- trimethoxybenzoate (TMB-8), ethylene glycol-bis$({/beta}-amino\;ethyl ether)-N,N,N'$, N'-tetra acetic acid (EGTA), and nifedifine partially blocked the inhibitory effects of ANG II on $Na^+$ uptake. When ANG II and bradykinin (BK) were treated together, $Na^+$ uptake was further reduced $(88.47{\pm}1.98%\;of\;that\;of\;ANG\;II,\;81.85{\pm}1.84%\;of\;that\;of\;BK)$. In addition, W-7 and KN-62 blocked the ANG II-induced inhibition of $Na^+$ uptake. Arachidonic acid reduced $Na^+$ uptake in a dose-dependent manner. When ANG II and arachidonic acid were treated together, inhibitory effects on $Na^+$ uptake significantly exhibited greater reduction than that of each group, respectively. When PTCs were treated by mepacrine $(10^{-6}\;M)$ and AACOCF3 $(10^{-5}\;M)$ for 1 hr before the addition of $(<10^{-9}\;ANG\;II)$, the inhibitory effect of ANG II was reversed. In addition, econazole $(>10^{-6}\;M)$ blocked ANG II-induced inhibition of $Na^+$ uptake. In conclusion, the $[Ca^{2+}]_i$ (calcium-calmodulin-dependent kinase) and phospholipase $A_2\;(PLA_2)$ metabolites are involved in the inhibitory effects of ANG II on $Na^+$ uptake in the PTCs.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.101-109
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• 2016

Reducing $[Mg^{2+}]_o$ to 0.1 mM can evoke repetitive $[Ca^{2+}]_i$ spikes and seizure activity, which induces neuronal cell death in a process called excitotoxicity. We examined the issue of whether cultured rat hippocampal neurons preconditioned by a brief exposure to 0.1 mM $[Mg^{2+}]_o$ are rendered resistant to excitotoxicity induced by a subsequent prolonged exposure and whether $Ca^{2+}$ spikes are involved in this process. Preconditioning by an exposure to 0.1 mM $[Mg^{2+}]_o$ for 5 min inhibited significantly subsequent 24 h exposure-induced cell death 24 h later (tolerance). Such tolerance was prevented by both the NMDA receptor antagonist D-AP5 and the L-type $Ca^{2+}$ channel antagonist nimodipine, which blocked 0.1 mM $[Mg^{2+}]_o$-induced $[Ca^{2+}]_i$ spikes. The AMPA receptor antagonist NBQX significantly inhibited both the tolerance and the $[Ca^{2+}]_i$ spikes. The intracellular $Ca^{2+}$ chelator BAPTA-AM significantly prevented the tolerance. The nonspecific PKC inhibitor staurosporin inhibited the tolerance without affecting the $[Ca^{2+}]_i$ spikes. While $G{\ddot{o}}6976$, a specific inhibitor of $PKC{\alpha}$ had no effect on the tolerance, both the $PKC{\varepsilon}$ translocation inhibitor and the $PKC{\zeta}$ pseudosubstrate inhibitor significantly inhibited the tolerance without affecting the $[Ca^{2+}]_i$ spikes. Furthermore, JAK-2 inhibitor AG490, MAPK kinase inhibitor PD98059, and CaMKII inhibitor KN-62 inhibited the tolerance, but PI-3 kinase inhibitor LY294,002 did not. The protein synthesis inhibitor cycloheximide significantly inhibited the tolerance. Collectively, these results suggest that low $[Mg^{2+}]_o$ preconditioning induced excitotoxic tolerance was directly or indirectly mediated through the $[Ca^{2+}]_i$ spike-induced activation of $PKC{\varepsilon}$ and $PKC{\xi}$, JAK-2, MAPK kinase, CaMKII and the de novo synthesis of proteins.