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임재명,오종민,박완철,한동준 경희대학교 환경연구소 1994 環境硏究 論文集 Vol.5 No.-
The composting process is a suitable to dispose the livestock manure in terms of resources recovery. However the performance of composting process is greatly affected by the environmental conditions such as characteristics of manure, type of the bulking agent, Initial moistuer contents, temperature, recycle and so on. The purpose of this study is to evaluate the optimum environmental conditions of composting process for livestock manure. The analytical results indicated that no bulking agent was necessary for the cow manure because of the proper C/N ratio. However the pig manure required a bulking agent since the pig manure had not only low in C/N ratio but poor ventilation characteristics. In addition, the initial moisture content for optimum composting appeared to be about 60%. The temperature control was also an essential factor to enhance the activity of thermophilic microorganisms in the laboratory composting unit. It was further found that the recycle of composts may contributed the completion of composting precess as well as C/N ratio reduction and moisture control.
The Roles of FGF-4 on the Differentiation of Trophoblast Stem (TS) Cells
최민규(Min-Kyu Choi),오정택(Jung-Taek Oh),오재민(Jay-Min Oh) 대한해부학회 2004 Anatomy & Cell Biology Vol.37 No.2
FGF-4는 세포의 증식, 분화, 이동, 침투, 혈관생성, 및 여러 세포에서 apoptosis를 포함한 stress에 대하여 세포를 보호하는 기능 등의 많은 작용을 가지고 있다. 그러나 이렇게 많은 기능을 가지고 있음에도 불구하고 태반이나 trophoblast에서 fibroblast growth factor-4 (FGF-4)의 역할에 대한 연구는 거의 없는 실정이다. 따라서 본 실험은 태반의 발달과정에서의 FGF-4의 역할에 대하여 알아보기 위하여 TS cell의 분화과정에 미치는 FGF-4의 역할을 조사하였다. Trophoblastic stem (TS) cell에 처리된 FGF-4는 48시간 후에 태반의 조기발달을 유도하는 Eomesodermine의 mRNA발현을 증가시켰고 태반발달과 정 중에 태반의 혈관형성에 중요한 역할을 하는 p38의 활성화와 Dlx-3의 발현을 유도 시켰을 뿐만 아니라 내피세포만 특이적으로 자랄 수 있는 firbinogen-thrombin gel에서 TS cell을 건강한 상태로 유지시켰다. 또한 extracellular-signal regulated kinase를 활성화 시키고 focal adhesion kinase의 활성을 억제 시킴으로써 TS cell의 분화를 억제하고 TS cell의 증식상태를 활발하게 유지하였다. 이러한 결과들을 종합하여 볼 때, FGF-4는 태반의 발달과정에 필요한 TS cells의 전 분화과정에 중요한 역할을 하리라고 생각한다. Fibroblast growth factor-4 (FGF-4) has various functions, affecting many signaling pathways, and leading to cellular proliferation and differentiation and to the regulation of cell migration, invasion, and angiogenesis. However, there are few reports of the relationship between TS cells and FGF-4 even if FGF-4 is located in inner cell mass of embryo and Fibroblast growth factor receptor (FGFR) is located in TS cells. Therefore the physiologic effects of FGF-4 on TS cells were investigated for identifying the effects of FGF-4 on TS ell differentiation. FGF-4 was involved in early stage development of the trophoblast via upregulation of eomesodermin mRNA expression. In addition, FGF-4 suppressed the differentiation of TS cells through activation of extracellular-signal regulated kinase (Erk) and suppression of focal adhesion kinase (FAK) activation, which in TS cells is an important indicator of early trophoblast cell differentiation, migration and invasion. FGF-4 was involved in angiogenesis in the trophoblast through the activation of p38 and the induction of Dlx-3 mRNA expression in TS cells. In addition, TS cells cultured with FGF-4 for 4 days in a thrombinfibrinogen gel culture system, a specific culture system for endothelial cells, showed a healthy appearance, while TS cells cultured without FGF-4 were severely damaged. Taken together, these data suggest that FGF-4 is closely involved in differentiation of TS cells for development of placenta.
A Central Pressor Response to Endogenous Nitric Oxide Synthesis Inhibition in Anesthetized Rats
Moon, Sung-Ho,Yang, Min-Joon,Oh, Seung-Ho,Kim, Mi-Won,Yoo, Kwang-Jay,Lee, Jong-Eun,Jun, Jae-Yeoul,Yeum, Cheol-Ho,Yoon, Pyung-Jin The Korean Physiological Society 1994 대한생리학회지 Vol.28 No.2
The present study was aimed to determine if endogenous L-arginine-nitric oxide (NO) pathway has central, rather than peripheral, mechanisms in blood pressure regulation. Arterial blood pressure and heart rate responses to acute inhibition of the t-arginine-NO pathway were examined in rats anesthetized with thiopental (50 mg/kg, IP). An intracerebroventricular (ICV) cannula was placed in the left lateral ventricle. The right femoral artery was cannulated to measure arterial blood pressure and the vein to serve as an infusion route. $N^G-nitro-L-arginine$ methyl ester (L-NAME) was infused either intracerebroventricularly or intravenously. ICV infusion $(1.25\;{\mu}L/min)$ of L-NAME $(20\;or\;100\;{\mu}g/kg)$ per minute for 60 min) increased the mean arterial pressure and heart rate. Plasma renin concentrations(PRC) were significantly lower in L-NAME-infused group than in the control. L-Arginine $(60\;{\mu}g/min,\;ICV)$ prevented the pressor response to ICV L-NAME. The pressor response was not affected by simultaneous intravenous infusion of saralasin, but was abolished by hexamethonium treatment. Intravenous infusion $(40\;{\mu}L/min,\;10{\sim}100\;{\mu}g/kg\;per\;minute\;for\;60\;min)$ also increased blood pressure, while it decreased heart rate. These results indicate that endogenous L-arginine-NO pathway has separate central and peripheral mechanisms in regulating the cardiovascular function. The central effect may not be mediated via activation of renin-angiotensin system, but via, at least in part, activation of the sympathetic outflow.
Role of IL-1α in Cisplatin-Induced Acute Renal Failure in Mice
( Jay Wook Lee ),( Woo Jin Nam ),( Min Jee Han ),( Jung Ho Shin ),( Jin Gun Kim ),( Su Hyun Kim ),( Hye Ryoun Kim ),( Dong Jin Oh ) 대한내과학회 2011 The Korean Journal of Internal Medicine Vol.26 No.2
Background/Aims: For unknown reasons, caspase-1 -/- mice, protected against cisplatin-induced acute renal failure (ARF), are deficient in interleukin (IL)-1α. We thus asked whether IL-1α deficiency underlies the mechanism of protection against cisplatin-induced ARF in these mice. Methods: Cisplatin (30 mg/kg) was injected intraperitoneally into wild-type C57BL/6 mice to produce a cisplatin-induced model of ARF. IL-1α was measured in control vehicle- and cisplatin-treated wild-type animals. We also examined whether IL-1α -/- mice were similarly protected against cisplatin-induced ARF. Additionally, infiltration of CD11b- and CD49b-positive cells, as markers of macrophages, natural killer, and natural killer T cells (pan-NK cells), was investigated in wild-type and IL-1α -/- mice. Results: Compared with vehicle-treated mice, renal IL-1α increased in cisplatin-treated wild-type mice beginning on day 1. IL-1α -/- mice were shown to be protected against cisplatin-induced ARF. No significant difference in the infiltration of neutrophils or CD11b- and CD49b-positive cells were observed between wild-type and IL-1α -/- mice. Conclusions: Mice deficient in IL-1α are protected against cisplatin-induced ARF. The lack of IL-1α may explain, at least in part, the protection against cisplatin-induced ARF observed in caspase-1 -/- mice. Investigation of the protective mechanism (s) in IL-1α -/- mice in cisplatin-induced ARF merits further study. (Korean J Intern Med 2011;26:187-194)