• Title/Summary/Keyword: VCM

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Effects of Metal Oxide Addition on Co-pyrolysis of PVC and ABS Mixtures (PVC와 ABS 혼합물의 공열분해에 대한 금속산화물의 첨가 효과)

  • Kim, Hee Taik;Choung, Youn Wook;Lee, Hae Pyeong
    • Applied Chemistry for Engineering
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    • v.16 no.2
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    • pp.296-303
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    • 2005
  • The co-pyrolysis characteristics of polyvinylchloride (PVC) and acrylonitrile butadiene styrene (ABS) mixtures with various mixing ratios and effect of addition of CaO and $Cu_2O$ have been studied using thermogravimetry (TG) and gas chromatograph-mass spectrometry (GC-MS). In an isothermal decomposition conducted at $500^{\circ}C$, the yields of styrene monomers and aromatic compounds increased as the mixing ratio of ABS increased, and the yield of BTX compounds reached its maximum (16.14%) when the mixing ratios of PVC and ABS was 4:1. In an isothermal decomposition added with metal oxides, the maximum yield of liquid product was 73% when CaO [CaO/(PVC+ABS)=0.4] was added and it was 70% when $Cu_2O$ [$Cu_2O$/(PVC+ABS)=0.4] was added, respectively, where HCl contained in the gaseous product was completely removed when added with CaO [CaO/(PVC+ABS)=0.5] and $Cu_2O$ [$Cu_2O$/(PVC+ABS)=1.0]. Therefore, to obtain the highest yield of liquid product it appears to be the reaction condition: the reaction temperature of $500^{\circ}C$ and mixing ratios of CaO and $Cu_2O$ are 0.5 and 1.0, respectively.

Improvement of infrared channel emissivity data in COMS observation area from recent MODIS data(2009-2012) (최근 MODIS 자료(2009-2012)를 이용한 천리안 관측 지역의 적외채널 방출률 자료 개선)

  • Park, Ki-Hong;Suh, Myoung-Seok
    • Korean Journal of Remote Sensing
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    • v.30 no.1
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    • pp.109-126
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    • 2014
  • We improved the Land Surface Emissivity (LSE) data (Kongju National University LSE v.2: KNULSE_v2) over the Communication, Ocean and Meteorological Satellite (COMS) observation region using recent(2009-2012) Moderate Resolution Imaging Spectroradiometer (MODIS) data. The surface emissivity was derived using the Vegetation Cover Method (VCM) based on the assumption that the pixel is only composed of ground and vegetation. The main issues addressed in this study are as follows: 1) the impacts of snow cover are included using Normalized Difference Snow Index (NDSI) data, 2) the number of channels is extended from two (11, 12 ${\mu}m$) to four channels (3.7, 8.7, 11, 12 ${\mu}m$), 3) the land cover map data is also updated using the optimized remapping of the five state-of-the-art land cover maps, and 4) the latest look-up table for the emissivity of land surface according to the land cover is used. The updated emissivity data showed a strong seasonal variation with high and low values for the summer and winter, respectively. However, the surface emissivity over the desert or evergreen tree areas showed a relatively weak seasonal variation irrespective of the channels. The snow cover generally increases the emissivity of 3.7, 8.7, and 11 ${\mu}m$ but decreases that of 12 ${\mu}m$. As the results show, the pattern correlation between the updated emissivity data and the MODIS LSE data is clearly increased for the winter season, in particular, the 11 ${\mu}m$. However, the differences between the two emissivity data are slightly increased with a maximum increase in the 3.7 ${\mu}m$. The emissivity data updated in this study can be used for the improvement of accuracy of land surface temperature derived from the infrared channel data of COMS.

The Role of Adenosine Receptors on Acetylcholine Release in the Rat Striatum

  • Kim, Do-Kyung;Kim, Hyeon-A;Choi, Bong-Kyu
    • The Korean Journal of Physiology and Pharmacology
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    • v.1 no.1
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    • pp.1-12
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    • 1997
  • As it has been reported that the depolarization induced acetylcholine (ACh) release is modulated by activation of presynaptic $A_1$ adenosine heteroreceptor and various evidence suggest that indicate the $A_2$ adenosine receptor is present in the striatum, this study was undertaken to delineate the role of adenosine receptors on the striatal ACh release. Slices from the rat striatum were equilibrated with $[^3H]$choline and then the release amount of the labelled product, $[^3H]$ACh, which was evoked by electrical stimulation (rectangular pulses, 3 Hz, 2 ms, 24 mA, $5\;Vcm^{-1}$, 2 min), was measured, and the influence of various agents on the evoked tritium outflow was investigated. And also, quantitative receptor autoradiography and drug-receptor binding assay were performed in order to confirm the presence and characteristics of $A_1$ and $A_2$ adenosine receptors in the rat striatum. Adenosine $(10{sim}100\;{mu}M)$ and $N^6$-cyclopentyladenosine (CPA, $1{sim}100\;{mu}M)$ decreased the $[^3H]$ACh release in a dose-dependent manner without changing the basal rate of release in the rat striatum. The reducing effects of ACh release by adenosine and CPA were abolished by 8-cyclopentyl-1,3-dipropy-Ixanthine (DPCPX, 2 ${mu}M$), a selective $A_1$, adenosine receptor antagonist, treatment. The effect of adenosine was potentiated markedly by 3,7-dimethyl-1-propargylxanthine (DMPX, 10 ${mu}M$), a specific $A_2$ adenosine receptor antagonist. 2-P-(2-carboxyethyl)phenethylamimo-5'-N- ethylcarboxamidoadenosine hydrochloride (CGS-21680C), in concentrations ranging from 0.01 to 10 ${mu}M$, a recently introduced potent $A_2$ adenosine receptor agonist, increased the $[^3H]$ACh release in a dose related fashion without changing the basal rate of release. These effects were completely abolished by DMPX $(10\;{mu}M)$. In autoradiograrhy experiments, $[^3H]$2-chloro-$N^6$-cyclopentyladenosine ($[^3H]$ CCPA) bindings were highly localized in the hippocampus and the cerebral cortex. Additionally, lower levels of binding were found in the striatum. However, $[^3H]$CGS-21680C bindings were highly localized in the striatal region with the greatest density of binding found in the caudate nucleus and putamen. Lower levels of binding were also found in the nucleus accumbens and olfactory tubercle. In drug-receptor binding assay, binding of $[^3H]$ CCPA to $A_1$ adenosine receptors of rat striatal membranes was inhibited by CPA ($K_i$ = 1.6 nM) and N-ethylcarboxamidoadenosine (NECA, $K_i$ = 12.9 nM), but not by CGS-21680C ($K_i$ = 2609.2 nM) and DMPX ($K_i$ = 19,386 nM). In contrast, $[^3H]$CGS-21680C binding to $A_2$ denosine receptors was inhibited by CGS-21680C ($K_i$ = 47.6 nM) and NECA ($K_i$ = 44.9 nM), but not by CPA ($K_i$ = 2099.2 nM) and DPCPX ($K_i$ = 19,207 nM). The results presented here suggest that both types of $A_1$ and $A_2$ adenosine heteroreceptors exist and play an important role in ACh release in the rat striatal cholinergic neurons.

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Influence of Adenosine and Magnesium on Acetylcholine Release in the Rat Hippocampus (흰쥐 해마에서 Acetylcholine 유리에 미치는 Adenosine 및 Magnesium의 영향)

  • Choi, Bong-Kyu;Yoon, Young-Bok
    • The Korean Journal of Pharmacology
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    • v.29 no.2
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    • pp.175-182
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    • 1993
  • As it has been reported that the depolarization-induced ACh release is modulated by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus and various lines of evidence indicate the adenosine effect is magnesium dependent, the present study was undertaken to delineate the role of endogenus adenosine as a modulator of hippocampal acetylcholine release in this study. Slices from the rat hippocampus were equilibrated with $[^3H]-choline$ and the release of the labelled product, $[^3H]-ACh$, was evoked by electrical stimulation(3Hz, $5\;V\;cm^{-1},$ 2ms, rectangular pulses), and the influence of various agents on the evoked tritium outflow was investigated. Adenosine, in concentrations ranging from $0.3\;to\;100\;{\mu}M$, decreased the $[^3H]-ACh$ release in a dose-dependent manner without changing the basal rate of release. $DPCPX(1{\sim}10{\mu}M)$, a selective $A_1-receptor$ antagonist, increased the $[^3H]-ACh$ release in a dose-related fashion with slight increase of basal tritium release. And the effects of adenosine were significantly inhibited by $DPCPX(2{\mu}M)$ treatment. CPCA, a specific $A_2-agonist$, in concentration ranging from $0.3\;to\;30\;{\mu}M$ decreased evoked tritium outflow with increase of basal rate of tritium release, and these effects were also abolished by $DPCPX(2{\mu}M)$ pretreatment. But, $CGS(0.1{\sim}10{\mu}M)$, a recently introduced potent $A_2-agonist$, did not alter the evoked tritium outflow. When the magnesium concentration of the medium was reduced to 0 mM, there was no change in evoked ACh release by adenosine. In contrast, increasing the magnesium concentration to 4 mM, the inhibitory effects of adenosine were significantly potentiated. These results indicate that $A_1-adenosine$ heteroreceptor is involved in ACh-release in the rat hippocampus and the inhibitory effects of adenosine mediated by $A_1-receptor$ is magnesium-dependent.

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