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염충호 ( Yeom Chung Ho ),최기철 ( Choe Gi Cheol ),이종은 ( Lee Jong Eun ),정종훈 ( Jeong Jong Hun ),전제열 ( Jeon Je Yeol ),윤평진 ( Yun Pyeong Jin ),염철호 ( Yeom Cheol Ho ) 대한신장학회 2001 Kidney Research and Clinical Practice Vol.20 No.6
2-kidney, 1 clip(2K1C) 신혈관성 고혈압 동물에서 생체내 내원성 산화질소(nitric oxide, NO)에 의한 혈관확장성 긴장이 변화되는가 밝히고자 NG-nitro-L-arginine(L-NNA), lipopolysaccharide(LPS) 및 tempol을 투여하여 혈압변화 및 혈장 NO 함량을, 그리고 적출 동맥환표본의 장력반응과 NO synthase(NOS) 단백발현을 조사하여 다음과 같은 결과를 얻었다. 1) L-NNA는 2K1C 고혈압군과 대조군에서 혈압을 상승시켰으며 그 정도는 양군에서 유사하였다. 2) LPS는 고혈압군과 대조군에서 혈압을 하강시켰고 그 정도는 양군에서 유사하였으며 고혈압군은 시간이 경과함에 따라 혈압이 회복된 양상을 보였다. 3) Tempol은 고혈압군에서 서서히 혈압을 하강시켰으나 대조군에서는 혈압변화를 일으키지 않았다. 4) LPS 투여 후 혈장 NO 함량은 고혈압군과 대조군에서 각각 유의하게 증가되었으며 양군간의 차이는 볼 수 없었다. 5) 혈장 NO 함량은 고혈압군과 대조군에서 tempol에 의해 영향 받지 않았다. 6) L-NNA에 의한 혈관수축반응은 고혈압군에서 대조군에 비해 유의하게 약화되었다. 7) 혈관에서 eNOS 및 iNOS 단백발현은 고혈압군에서 대조군에 비해 각각 유의하게 낮았다. 이상의 실험결과로 보아 2K1C 신혈관성 고혈압에서 생체내 NO의 총 혈관확장성 긴장은 변하지 않으나 혈관에서의 NO 긴장은 감소될 것으로 사료된다. Endogenous nitric oxide(NO) plays an important role in the regulation of blood pressure. It has been known that the evoked NO-dependent dilator system may be impaired in various hypertensive models. The effects of NG-nitro-L-arginine(L-NNA), lipopolysaccharide( LPS) and tempol on mean arterial pressure( MAP) and the effects of L-NNA on isolated aorta tone were studied in order to elucidate potential alterations in resting vasodilator tone of NO in two-kidney, one clip(2K1C) hypertension. Plasma nitrite/ nitrate levels were measured by colorimetric assay, and the expression of endothelial and inducible NO synthases(eNOS, iNOS) was determined by Western blot analysis. L-NNA caused an increase of MAP, while LPS produced a hypotensive effect in both 2K1C and control rats. The magnitude of the pressor or depressor response to L-NNA and LPS was comparable in the two groups. Tempol induced a sustained decrease in MAP in 2K1C rats, while it had no effects on MAP in control rats. Plasma concentrations of NO metabolites were significantly increased following the LPS-treatment in both 2K1C and control rats, while they were not affected by tempol-treatment. In endothelium-intact aortic rings precontracted with 25 mM KCl, L-NNA caused a dose-dependent contraction. The magnitude of the maximal contraction was attenuated in 2K1C rats as compared with control. An inhibition of contractile responses to L-NNA in the hypertensive group was also shown in rubbed rings, although the magnitude of contractions was markedly reduced. The vascular expression of both eNOS and iNOS was significantly decreased in 2K1C rats as compared with control. These results indicate that 2K1C hypertension is associated with a reduced basal vasodilator tone of NO and a decrease in the vascular expression of NOS isozymes.
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Mice 소장의 Cajal 세포에서 기록되는 향도잡이 전류의 특성
장성종 ( Jang Seong Jong ),조은택 ( Jo Eun Taeg ),허광식 ( Heo Gwang Sig ),박찬국 ( Park Chan Gug ),김만우 ( Kim Man U ),장인엽 ( Jang In Yeob ),신무경 ( Sin Mu Gyeong ),차경훈 ( Cha Gyeong Hun ),염철호 ( Yeom Cheol Ho ),전제열 ( 대한소화기학회 2003 대한소화기학회지 Vol.42 No.2
Background/Aims: Gastrointestinal motility is initiated by the periodic generation of slow waves. Interstitial cells of Cajal (ICC) are pacemaker cells that generate slow waves and drive spontaneous mechanical contractions of the gastrointestinal smooth muscle. Slow waves generate the periodic activation of spontaneous inward currents (pacemaker currents). The aim of this study was to investigate the characterization of pacemaker currents of ICC. Methods: The ICC in mice small intestine were cultured with stem cell factor for 2 days, and then we recorded pacemaker currents and slow waves using a whole-cell patch clamp technique. Results: Under voltage clamp at -80 mV of holding potential, ICC generated pacemaker currents. Tetrodotoxin and nifedipine did not affect on the pacemaker currents. In addition, tetraethylammonium, 4-aminopyridine and glibenclamide did not affect on the pacemaker currents. The reduction of external Na+ concentrations inhibited pacemaker currents. Moreover, these currents were completely abolished in the external Ca2+-free condition. Gadolinium and flufenamic acid, inhibitors of non-selective cationic currents, inhibited pacemaker currents. Thapsigargin and cyclopiazoic acid, inhibitors of Ca2+-ATPase in endoplasmic reticulum, abolished pacemaker currents. Carbachol depolarized membrane potential and increased inward currents. Conclusions: These results suggest that pacemaker currents are mediated by the activation of non-selective cation channel and become a target of neurotransmitters in regulation of intestinal motility. (Korean J Gastroenterol 2003;42:121-127)
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염철호,김재백 圓光大學校 藥品硏究所 1987 藥品硏究所報 Vol.2 No.1
Time-dependent pharmacokinetics for rifampicin, a drug commonly used in the treatment of mycobacterium tuberculosis, was studied in 9 male and 4 female tuberculous patients. Rifampicin (600㎎) was administered oralIy every morning before breakfast over a period of 8 weeks, combined with isoniazid (300㎎) , ethambutol (800 ㎎) and pyridoxine(500㎎). On the 1st, 14th, 21st, 28th and 56th days of treatment, venous blood samples were drawn 1,2,4 and 8 hours after the administration of rifampicin. Rifampicin concentration in the serum was determined by high-performance liquid chromatography at 254 nm. Maximum blood concentration(Cmax ), area under blood concentration curve(AUC), biological half-life (t1/2), apparent volume of distribution (Vd), total clearance (CI _tot) and first-pass effect were calculated from data of the serum rifampicin concentrations. Pharmacokinetics of rifampicin in patients was interpreted by one-compartment model The results obtained were summarized as follows : 1 . Cmax and AUC gradually decreased until the 21st day of treatment and, thereafter reached a steady-state until the 56th day of treatment. 2. Vd,Cl_tot and first-pass effect showed a definite increase up to the 28th day of treatment. After that, they reached a steady- state until the 56th day of treatment. 3 Hioioglcai half-life fluctuated until the 29th day of treatment and reached a steady- state on the day 28. In conclusion, pharmacokinetics of rlfampicin was found to be time-dependent when administrered orally in combination with isoniazid, ethambutol and pyridoxine.
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