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알루미늄 Droplets 합체거동에 미치는 Salt Flux 및 합금원소 첨가의 영향
김예식 ( Ye Sik Kim ),윤의박 ( Eui Pak Yoon ),김기태 ( Ki Tae Kim ),정운재 ( Woon Jae Jung ),조덕호 ( Duk Ho Jo ) 한국주조공학회 2000 한국주조공학회지 Vol.20 No.1
The remelting for recycling of thin aluminum scrap, such as aluminum chip generally involves melting of these pieces sub-merged in molten salt flux. In this study, the effects of salt flux compositions and alloying elements on the aluminum dropletscoa-lescence and oxide film removal were studied in 99.8%A1, Al-1.01%Cu, Al-1.03%Si, and Al-1.38%Mg alloys as a function of holding time at 740℃ Salt fluxes based on NaC1-KCl(1:1) with addition of 5wt.% fluorides(NaF, Na3AlF6, CaF2) or 5 Wt.% chloride(MgCl2, AlCl3) were used. The experimental results show that NaCl-KCl(1:1)with addition of 5 wt.% fluorides exhibits better coalescence ability than that with chlorides. The oxide film is not removed by NaCl-KCl(1:1) with addition of 5 wt.% chlorides, while it is removed by NaCl-KCl(1:1) with addition of 5 wt.% fluorides. The aluminum droplets coalescence and oxide film removal by salt fluxes are related to interfacial tension between metal and salt flux.
Calcium 및 Potassium 이 적출 이자 [ 췌장 (膵臟) ] 의 효소유리에 미치는 영향
김경환 ( Kyung Hwan Kim ),안영수 ( Young Soo Ahn ),이선미 ( Sun Mee Lee ),김동구 ( Dong Goo Kim ),홍사석 ( Sa Suk Hong ),김예식 ( Ye Sik Kim ) 대한소화기학회 1988 대한소화기학회지 Vol.20 No.2
N/A Stimulation of cholinergic receptors of pancreatic acinar cells results in enzyme secretion. The first consequence of this stimulation-secretion coupling is a rapid increase in the concentration of cytoplasmic free calcium. However, the cytoplasmic Ca2+ returns to the prestimulated level during the sustained stimulation of the gland, which implicates that the extracellular C2+ might be of importance for the sustained secretion. Furthermore, it is suggested that in the mechanism of Ca2+-mediated enzyme secretion, Na2+, K+ -pump may be involved, but K+ stimulated enzyme secretion is apparent only at high concentration. Present study was undertaken to clarify the role of extracellular C2+ and K+ on the basal and acetylcholine-stimulated enzyme secretion of pancreas. Baby rats weighing 70-100 g of either sex were used. After decapitation, uncinate process of pancreas was isolated. The pieces of pancreata were incubated in Krebs-Ringer bicarbonate buffer (KRBB) and the concentration of Ca2+ in the incubation medium was changed from 0 to 10.5 mM and that of K+ from 0 to 120 mM. Acetylcholine (10-6M) was added to the incubation medium to stimulate enzyme release. The results obtained are summarized as follows: 1) The basal amylase release from the pancreatic slice in the normal KRBB was fairly constant, and repeated stimulation with acetylcholine(10 -6M) increased the amylase release persistently. 2) Increase of calcium concentration in the incubation media enhanced both basal and stimulated amylase releases in a concentration-dependent manner. However, higher concentration of calcium (10.5 mM) inhibited the stimulated amylase release. 3) Reduction of the Ca concentration caused decrease of the stimulated amylase release, but there was little change in basal amylase release. 4) In Ca2+-free media, the acetylcholine-induced amylase release was increased only during the first stimulation, and thereafter there was little response to the repeated stimulation. The basal amylase release was not changed in calcium-free media. 5) Basal amylase release from the pancreatic slice was increased by increasing the concentration of K+ in a concentration-dependent manner upto 60mM. However, the stimulated secretion was not affected by changing K+ concentrations. 6) In K+ free media, stimulated amylase release was markedly suppressed, but basal amylase secretion was not affected. 7) Increase of basal amylase release by 60 mM K+ was completely suppressed by atropine(10 -6M). From these results, it is suggested that intracellular calcium is utilized in the basal and in the initial phase of stimulated enzyme secretion of pancreas, however extracellular calcium is important for the sustained stimulation of pancreatic enzyme secretion. It is also suggested that potassium plays a supportable role in Ca-mediated enzyme secretion, and high extracellular K+-induced enzyme secretion may be mediated by increasing the release of cholinergic neurotransmitter.
아드레나린성 약물이 유문부결찰 백서의 위분비 기능에 미치는 영향
홍사석(Sa Suk Hong),김학산(Hak San Kim),김예식(Ye Sik Kim),김동구(Dong Goo Kim) 대한소화기학회 1987 대한소화기학회지 Vol.19 No.1
N/A Gastric secretion is modulated largely by three major factors-the autonomic nervous system, the gastrointestinal hormones and the circulation. For autonomic nervous system, the parasympathetic influence on gastric secretion has been widely studied. However, the influence of sympatho-adrenal system has received much less attention and its role on gastric secretion remains a matter of controversy. Present investigation was undertaken to evaluate the adrenergic influence on gastric secretion using the experimental model of pylorus-ligated rat. Immediately after pylorus ligation intrinsic or synthetic adrenergic agents (methoxamine, norepinephrine, epinephrine, isoproterenol or dopamine) were injected subcutaneously. After 3-or 6-hour period of pyloric ligation the stomach was removed and gastric juice was collected for the evaluation of gastric secretory function. And blood glucose level was also measured. The results obtained are as folllows. 1) Gastric secretory function was active in the group of 3 hours pyloric-ligation and depressed greatly therafter. 2) All adrenergic drugs used in this experirnent suppressed the volume of gastric juice and acid output. The degree of suppression was marked in epinephrine or isoproterenol, moderate in methoxamine or norepinephrine and minimal in dopamine treated rats. 3) Blood glucose level was not directly correlated with the suppressive action of adrenergic drugs on gastric secretion. From the above results it is concluded that gastric secretory function is suppressed by adrenergic influence. And it is suggested that adrenergic beta-receptor acitivation plays a major role in the suppression of gastric secretion.