• Journal of the Korean Recycled Construction Resources Institute
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• v.6 no.4
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• pp.119-126
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• 2012

Portland cement production-1.5billion tonnes yearly worldwide-contributes substantially to global atmospheric pollution(7% of total of $CO_2$ emissions). Attempts to increase the utilization of fly ash, by-products from thermal power plant to partially replace the cement in concrete are gathering momentum. But most of fly ash is currently dumped in landfills, thus creating a threat to the environment. Many researches on alkali-activated concrete that does not need the presence of cement as a binder have been carried out recently. Instead, the sources of material such as fly ash, that are rich in Silicon(Si) and Aluminium(Al), are activated by alkaline liquids to produce the binder. Hence concrete with no cement is effect reduction of $CO_2$ gas. In this study, we investigated the influence of the compressive strength of mortar on alkaline activator and curing condition in oder to develop cementless fly ash based alkali-activated concrete. In view of the results, we found out that it was possible for us to make alkali-activated mortar with 70MPa at the age of 28days by using alkaline activator manufactured as 1:1 the mass ratio of 9M NaOH and sodium silicate and applying the atmospheric curing after high temperature at $60^{\circ}C$ for 48hours.

• Journal of the Korean Recycled Construction Resources Institute
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• v.8 no.1
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• pp.33-40
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• 2013

The cement industry brought very severe environment problems with massive carbon dioxide during its production. To solve this problem, attempts on Alkali-Activated Slag (AAS) concrete that perfectly substitutes industrial by-products such as ground granulated blast furnace slag (GGBFS) for cement are being actively made. AAS concrete is possible to have high strength development at room temperature, however, it is difficult to ensure the working time due to the fast setting time and the loss of workabillity because of the alkali reaction. In this study, the early age properties of alkali activated slag mortar are investigated to obtain the fundamental data for AAS concrete application to structural members. The water-binder ratio (W/B) was fixed at 0.35 and sodium hydroxide and waterglass as alkali activator was used. The compressive strength, the flow and the ultrasonic pulse velocity were measured according to the type of superplasticisers, which were naphthalene(N), lignin(L), melamine(M) and PC(P), up to a maximum of 2 percent by the mass of GGBFS. The results showed that adding melamine type of superplasticizer improved the fluidity of AAS mortar without decreasing the compressive strength, while naphthalene and polycarbonate type of superplasticizer had little effect on the fluidity of AAS mortar.

• Resources Recycling
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• v.19 no.4
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• pp.19-28
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• 2010

Attempts to increase the utilization of a by-products such as fly ash and blast furnace slag to partially replace the cement in concrete are gathering momentum. But most of by-products is currently dumped in landfills, thus creating a threat to the environment. Many researches on alkali-activated concrete that does not need the presence of cement as a binder have been carried out recently. However, most study deal only with alkali-activated blast furnace slag or fly ash, as for the combined use of the both, little information is reported. In this study, we investigated the influence of mixture ratio of fly ash/slag, type of alkaline activator and curing condition on the workability and compressive strength of mortar in oder to develop cementless alkali-activated concrete. In view of the results, we found out that the mixture ratio of fly ash/slag and the type of alkaline activator always results to be significant factors. But the influence of curing temperature in the strength development of mortar is lower than the contribution due to other factors. At the age of 28days, the mixture 50% fly ash and 50% slag activated with 1:1 the mass ratio of 9M NaOH and sodium silicate, develop compressive strength of about 65 MPa under $20^{\circ}C$ curing.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.3
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• pp.229-239
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• 2009

The aim of the present study was to examine the effect of provinol, which is a mixture of polyphenolic compounds from red wine, on the secretion of catecholamines (CA) from isolated perfused rat adrenal medulla, and to elucidate its mechanism of action. Provinol (0.3 ${\sim}$ 3 ${\mu}g/ml$) perfused into an adrenal vein for 90 min dose- and time-dependently inhibited the CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic $N_N$ receptor agonist, 100 ${\mu}M$) and McN-A-343 (a selective muscarinic $M_1$ receptor agonist, 100 ${\mu}M$). Provinol itself did not affect basal CA secretion. Also, in the presence of provinol (1 ${\mu}g/ml$), the secretory responses of CA evoked by Bay-K-8644 (a voltage-dependent L-type dihydropyridine $Ca^{2+}$ channel activator, 10 ${\mu}M$), cyclopiazonic acid (a cytoplasmic $Ca^{2+}$-ATPase inhibitor, 10 ${\mu}M$) and veratridine (an activator of voltage-dependent $Na^+$ channels, 10 ${\mu}M$) were significantly reduced. Interestingly, in the simultaneous presence of provinol (1 ${\mu}g/ml$) plus L-NAME (a selective inhibitor of NO synthase, 30 ${\mu}M$), the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclpiazonic acid recovered to the considerable extent of the corresponding control secretion in comparison with the inhibition of provinol-treatment alone. Under the same condition, the level of NO released from adrenal medulla after the treatment of provinol (3 ${\mu}g/ml$) was greatly elevated in comparison to its basal release. Taken together, these data demonstrate that provinol inhibits the CA secretory responses evoked by stimulation of cholinergic (both muscarinic and nicotinic) receptors as well as by direct membrane-depolarization from the perfused rat adrenal medulla. This inhibitory effect of provinol seems to be exerted by inhibiting the influx of both calcium and sodium into the rat adrenal medullary cells along with the blockade of $Ca^{2+}$ release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of nitric oxide synthase.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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• pp.517-526
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• 2009

The present study was attempted to investigate whether polyphenolic compounds isolated from wine, which is brewed from Rubus coreanum Miquel (PCRC), may affect the release of catecholamines (CA) from the isolated perfused adrenal medulla of the spontaneously hypertensive rats (SHRs), and to establish its mechanism of action. PCRC $(20\sim180\;{\mu}g/ml)$ perfused into an adrenal vein for 90 min relatively dose-dependently inhibited the CA secretory responses to ACh (5.32 mM), high $K^+$ (56 mM), DMPP $(100\;{\mu}M)$ and McN-A-343 $(100\;{\mu}M)$. PCRC itself did not affect basal CA secretion (data not shown). Also, in the presence of PCRC $(60\;{\mu}g/ml)$, the CA secretory responses to veratridine (a selective $Na^+$ channel activator $(10\;{\mu}M)$, Bay-K-8644 (a L-type dihydropyridine $Ca^{2+}$ channel activator, $10\;{\mu}M$), and cyclopiazonic acid (a cytoplasmic $Ca^{2+}$-ATPase inhibitor, $10\;{\mu}M$) were significantly reduced, respectively. In the simultaneous presence of PCRC $(60\;{\mu}g/ml)$ and L-NAME (an inhibitor of NO synthase, $30\;{\mu}M$), the inhibitory responses of PCRC on the CA secretion evoked by ACh, high $K^+$, DMPP, and Bay-K-8644 were considerably recovered to the extent of the corresponding control secretion compared with that of PCRC-treatment alone. The level of NO released from adrenal medulla after the treatment of PCRC $(60\;{\mu}g/ml)$ was greatly elevated compared with the corresponding basal level. Taken together, these results demonstrate that PCRC inhibits the CA secretion from the isolated perfused adrenal medulla of the SHRs evoked by stimulation of cholinergic receptors as well as by direct membrane-depolarization. It seems that this inhibitory effect of PCRC is mediated by blocking the influx of calcium and sodium into the adrenal medullary chromaffin cells of the SHRs as well as by inhibition of $Ca^{2+}$ release from the cytoplasmic calcium store at least partly through the increased NO production due to the activation of NO synthase.

• Journal of the Korean Recycled Construction Resources Institute
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• v.10 no.2
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• pp.159-167
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• 2022

The present study assessed the micro structure and durability characteristics of ternary blended cement with different types of alkali activators. Ground granulated blast furnace slag(GGBS) and ferronickel slag(FNS) was replaced until 50 % of the weight of cement. In addition, potassuim hydroxide and sodium hydroxide were used for comparing the properties of different type of alkali activator. Ternary blended cement with alkali activators showed higher peak portlandite peak than that of OPC(Ordinary Portlande Cement) and non activated ternary blended cement. Also, there was no new hydration products in ternary blended cement or/and alkali activators. Based on the mercury intrustion porosimetry(MIP) test result, ternary blended cement increased macro pore while alkali activated ternary blended cement modified pore structure and increased microp pore as compared to OPC as control. Combination with alkali activators is desirable to enhance the compressive strength and freeze thaw resistance.

• Journal of the Korea Concrete Institute
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• v.23 no.4
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• pp.487-494
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• 2011

In this research, the possibility of using bottom ash as a binder for the alkali-activated cement mortar is studied. Several experiments were performed to investigate the variation of the material properties according to the mix proportion. In the experimental program, the flowability and compressive strength were evaluated for various values of water/ash ratio, activator/ash ratio, sodium silicate to sodium hydroxide ratio, curing temperature, and the fineness of bottom ash as the main variables. The experimental results showed that high strength of 40 MPa or greater could be achieved in $60^{\circ}C$ high temperature curing condition with proper flowability. For $20^{\circ}C$ ambient temperature curing, the 28 days compressive strength of approximately 30MPa could be obtained although the early-age strength development was very slow. Based on the results, the range of optimized mix design of bottom-ash based alkali-activated cement mortar was suggested. In addition, using the artificial neural network analysis, the flowability and compressive strength were predicted with the difference in the mix proportion of the bottom-ash based alkali-activated cement mortar.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.181-190
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• 1994

Endothelium-derived relaxing factor (EDRF) activates guanylate cyclase which mediates the formation of cGMP from GTP in vascular smooth muscle. It is well known that endothelium-dependent relaxation is impaired in spontaneously hypertensive rats (SHR). However, it is still unknown whether the impaired endothelium-dependent relaxation in SHR results from the reduced release of EDRF or from the decrease of vascular response to EDRF. We investigated the effects of cGMP on the contractility and Ca movement in the aorta of SHR and Wistar-Kyoto rats (WKY). The amplitude of the endothelium-dependent relaxation to actylcholine (ACh) was significantly less in SHR than in WKY. L-arginine $(10^{-3}M)$ did not increase endothelium-dependent relaxation in both strains. Sodium nitroprusside (SNP), an activator of guanylate cyclase, relaxed the 40 mM $K^+-induced$ contraction in a dose-dependent manner $(10^{-10}{\sim}10^{-6}\;M)$ in the endothelium-rubbed aortic strips of both strains. However, there was no significant difference in these relaxations between WKY and SHR. 8-bromo-cyclic guanosine monophosphate (8-Br-cGMP), a cell membrane-permeable derivative of cGMP relaxed the 40 mM $K^+-induced$ contraction in a dose-dependent manner $(10^{-6}{\sim}10^{-4}\;M)$ in the endothelium-rubbed aortic strips of both strains. Also norepinephrine $(10^{-6}\;M)-induced$ contractions in normal and Ca-free Tyrode's solution were suppressed by the pretreatment with 8-Br-cGMP $(10^{-4}\;M)$ in either strain. However, the amplitudes of suppression induced by 8-Br-cGMP were greater in SHR than that in WKY. Basal $^{45}Ca$ uptake and 40mM $K^+-stimulated\;^{45}Ca$ uptake were not suppressed by pretreatment with 8-Br-cGMP $(10^{-4}\;M)$ in single aortic smooth muscle cells of both SHR and WKY. From the above results, it is suggested that cGMP decreases Ca sensitivity in vascular smooth muscle cells and that the impaired endothelium-dependent relaxation in the aortic strips of SHR is not the result of a reduced vascular response to EDRF.

• Journal of the Korea institute for structural maintenance and inspection
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• v.20 no.5
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• pp.75-84
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• 2016

This paper presents an investigation of the mechanical properties on non-sintered cement pastes immersed in sea waters at three different temperatures. The non-sintered cement pastes were synthesized using blended binder(Class F fly ash; FA and ground granulated blast furnace slag; GGBFS) and alkali activator(sodium hydroxide and sodium silicate). Binders were prepared by mixing the FA and GGBFS in different blend weight ratios of 6:4, 7:3 and 8:2. The alkali activators were used 5wt% of blended binder, respectively. Calcium carbonate was used as an chemical additive. The compressive strength, bulk density and absorption of alkali-activated FA-GGBFS blends pastes were measured at 3 and 28 days after immersed in sea waters at three different temperatures($5^{\circ}C$, $15^{\circ}C$ and $25^{\circ}C$). The XRD and SEM tests of the pastes were conducted at 28 days. Water-soluble chloride(free chloride) and acid-soluble chloride(total chloride) contents in the pastes were also measured after 28 days immersion in sea water. The experimental results showed that increasing the content of FA in alkali-activated FA-GGBFS blends pastes immersed in sea water increases the absorption, water-soluble chloride content and acid-soluble chloride content, and reduces the compressive strength and bulk density. And it was found that there was a variation of strength change for the alkali-activated FA-GGBFS blends pastes immersed in sea waters at three different temperatures that depends on the blending ratio of FA and GGBFS.

• The Korean Journal of Pharmacology
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• v.32 no.2
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• pp.189-199
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• 1996

Myocardial ${\alpha}_1-adrenoceptors$ have been shown to mediate a biphaslc inotropic response that was characterized by a transient decline followed by a sustained increasing phase in guinea pig ventricular muscle. Recently one group reported that an ${\alpha}_1-adrenoceptors-induced$ intracellular $Na^+$ decrease is linked to fast $Na^+$ channel inhibition and another group reported that it is linked to $Na^+$-$K^+$ pump activation by ${\alpha}_{1b}-adrenoceptors$. But until now, its mechanism is not clear. Therefore, to see whether the $Na^+$channel or $Na^+-K^+$ pump is related to a decrease in intracellular $Na^+$ activity and/or the negative inotropic response, and which ${\alpha}_1-adrenoceptor$ subtype was involved in the decrease in intracellular $Na^+$activity by phenylephrine, we used conventional and sodium selective microelectrodes, and tension transducer to determine the effects of ${\alpha}_1-adrenergic$ stimulation on membrane potential, intracellular $Na^+$ activity, and twitch force in guinea pig ventricular muscles. $10^{-5}$ M Phenylephrine produced a slight hyperpolarization of the diastolic membrane potential, a decrease or increase in $a_N^i_a$, and a biphasic inotropic response. The negative inotropic response accompanied by a decrease in intracellular $Na^+$activity, whereas in muscles showing a remarkable positive inotropic response without initial negative inotropic effect was accompanied by an increase in intracellular $Na^+$ activity. The decrease in intracellular $Na^+$ activity was apparently inhibited by WB4101, an antagonist of the ${\alpha}_{1a}-adrenoceptors$. The decrease in intracellular $Na^+$ activity caused by phenylephrine was not abolished or reduced by a block of the fast $Na^+$ channels. $V_{max}$ also was not affected by phenylephrine. Phenylephrine produced an increase in intracellular $Na^+$ activity in the presence of a high concentration of extracellular $Ca^{2+}$ (in quiescent muscle) or phorbol dibutyrate, a protein kinase C activator(in beating muscle). These suggest that the ${\alpha}_{1a}-adrenoceptors-mediated$ decrease in intracellular $Na^+$ activity may be related to the protein kinase C.