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층류 확산화염에서의 매연과 질소산화물의 배출특성 : 공기측/연료측 희석제 첨가에 따른 영향
이종호,엄재호,박철웅,전충환,장영준,Lee, Jong-Ho,Eom, Jae-Ho,Park, Chul-Woong,Jun, Chung-Hwan,Jang, Young-June 대한기계학회 2003 大韓機械學會論文集B Vol.27 No.5
Present study has been conducted to see the relative effects of adding N: to fuel-side and air-side on flame structure, soot formation and NOx emissions. Experiments were carried out to ascertain to what degree chemical kinetics and/or molecular transport effects can explain the differences in soot formation and NOx emission by studying laminar diffusion flames. Direct photograph was taken to see the flame structure. CARS techniques was used to get the flame temperature profiles. And spatial distribution of soot could be obtained by PLII method. CHEMKIN code was also used to estimate the global residence time to predict NOx emissions at each condition. Results from these studies indicate that fuel-side dilution is more effective than air-side dilution in view of NOx emissions. However, air-side dilution shows greater effectiveness over fuel-side dilution in soot formation. And turbulent mixing and heat transfer problems were thought to be considered in practical applications.
리튬으로 유발된 신성 요붕증 흰쥐에서 Hydrochlorothiazide 투여 후 Aquaporin-2 발현의 변화
오윤규 ( O Yun Gyu ),이재욱 ( Lee Jae Ug ),장혜련 ( Jang Hye Lyeon ),박영선 ( Park Yeong Seon ),김근호 ( Kim Geun Ho ),한진석 ( Han Jin Seog ),엄재호 ( Eom Jae Ho ) 대한신장학회 2004 Kidney Research and Clinical Practice Vol.23 No.1
배 경 : 리튬은 신성 요붕증을 일으키는 대표적인 약물로 최근 리튬으로 인한 신성 요붕증에서 aquaporin-2 (AQP2)의 발현이 감소한다는 사실이 밝혀졌다. 한편 thiazide 이뇨제는 신성 요붕증 환자에서 요량을 감소시키는 효과가 있어 치료에 이용되고 있으나 정확한 기전은 밝혀지지 않고 있다. 방 법 : 저자들은 신성 요붕증에서 hydrochlorothiazide (HCTZ)의 항이뇨 효과의 기전을 밝히기 위하여 리튬을 1일 40 m㏖/㎏가 되게 5주간 투여하여 신성 요붕증을 유발한 흰쥐에서 HCTZ 3.75 ㎎/day를 osmotic minipump를 이용하여 마지막 1주간 투여한 후 반정량적immunoblotting과 면역조직화학법을 이용하여 AQP2의 발현을 알아보았다. 결 과 : 리튬 투여 후 HCTZ를 투여한 군 (Li+TZ)은 리튬만 투여한 군 (Li)에 비해 요량이 유의하게 감소하였고 (Li+TZ:45±11 mL/day vs. Li:127±1 mL/day, p<0.05), 요삼투질 농도는 유의하게 증가하였다 (Li+TZ:557±139 m㏖/㎏ vs. Li:207±9 m㏖/㎏ H₂O, p<0.05), 반정량적 immunoblotting에서 AQP2 단백 발현은 리튬 투여 후 대조군 (Control)에 비해 현저하게 줄었으나 Li+TZ군에서 Li군에 비해 유의하게 증가하였다 (Li+TZ:39±2% vs. Li:20±9%, p<0.05, of Control). 면역조직화학법에서 리튬을 투여한 두 군 (Li+TZ와 Li)에서 모두 Control에 비해 AQP2가 약하게 염색되었으나 Li+TZ에서 Li에 비해 강하게 염색되었다. 결 론 : 리튬으로 유발된 신성 요붕증에서 HCTZ는 요농축능과 AQP2 단백 발현을 부분적으로 증가시켰으며, HCTZ에 의한 AQP2 단백의 증가는 요농축능의 회복과 관련이 있을 것으로 생각한다. Background : Thiazides have been used in nephrogenic diabetes insipidus (NDI) patients to decrease urine volume, but the mechanism of antidiuretic effect is not known yet. Recently, it has been demonstrated that abundance of aquaporin-2 (AQP2) was decreased in lithium induced NDI. We performed this study to investigate the effect of hydrochlorothiazide (HCTZ) in lithium induced NDI rats and the change of AQP2 expression. Methods : NDI was induced in 7 male Spraque-Dawley rats by feeding lithium carbonate containing rat chow (40 mmol/㎏) for 5 weeks, 4 rats were control group. HCTZ 3.75㎎/day (n=3 among lithium treated; Li+TZ) or vehicle (n=4 among lithium treated and control; Li and Control, respectively) was infused to the rats through osmotic minipump for the last 7 days. Urine volume and urine osmolality were measured. Kidneys were processed for immunohistochemistry and immunoblotting using antibody to AQP2. Results : Li+TZ showed decreased urine volume (46±11 mL/day for Li+TZ vs. 127±1 mL/day for Li, p<0.05) and higher urine osmolality (557±139 mmol/㎏H₂O for Li+TZ vs. 207±9 mmol/㎏H₂O for Li, p<0.05) comparing to Li. In semi-quantitative immunoblotting using whole kidney homogenate, Li+TZ showed increase in AQP2 expression comparing to Li (39±2% for Li+TZ vs. 20±9% for Li p<0.05,% of normal controls). In immunohistochemistry, AQP2 expression in cortex was markedly decreased after lithium treatment. But, AQP2 expression was slightly increased after HCTZ treatment. Conclusion : HCTZ treatment partially increased urine concentrating ability and AQP2 expression in rats with lithium induced NDI. We concluded that partial improvement in urine concentrating ability might be associated with upregulation of AQP2. (Korean J Nephrol 2004;23(1):5-11)