• 대한환경공학회지
• /
• 제35권1호
• /
• pp.45-56
• /
• 2013

본 연구는 낙동강수계의 잔류의약물질을 관리하기 위한 기초자료로 제시되었다. 낙동강 본류에서 Iopromide는 $0.0015{\sim}0.37{\mu}g/L$, Mefenamic acid은 $0.0087{\sim}0.056{\mu}g/L$, Diclofenac은 $N.D.{\sim}0.01{\mu}g/L$, Atenolol은 $N.D.{\sim}0.024{\mu}g/L$, Propranolol은 $N.D.{\sim}0.0038{\mu}g/L$, Lincomycin은 $0.0005{\sim}0.038{\mu}g/L$, Trimethoprim은 $N.D.{\sim}0.0083{\mu}g/L$의 농도범위로 검출되었다. 유역의 하수처리장에서는 대부분 고농도로 검출되었으며, 특히 Iopromide가 최고 $5.38{\mu}g/L$까지 검출되었다. 축산폐수처리장에서는 린코마이신이 최고 $477{\mu}g/L$로 가장 높게 검출되었다. 조사결과, 낙동강 본류에서 의약물질은 구미하수처리장과 대구 금호강의 유입으로 농도가 높아져 인구 산업밀집지역의 영향이 큰 것으로 판단된다. 따라서 낙동강의 잔류의약물질을 효율적으로 관리하기 위해서는 금호강과 하 폐수처리장을 지속적으로 모니터링하고 관리하는 것이 바람직한 것으로 사료된다.

• 동아시아식생활학회지
• /
• 제15권1호
• /
• pp.49-56
• /
• 2005

The purpose of this study was to measure the changes of regional cerebral blood flow(rCBF) and blood pressure(BP) in rats, following the intravenous injection of Nelumbo nucifera water extract. The measurement was continually monitored by laser-doppler flowmeter and pressure transducer in anesthetized adult Sprague-Dawley rats for about 2 to 2 and half hours through the data acquisition system composed of MacLab and Macintosh computer. The results of this experiment were as follows. Nelumbo nucifera significantly increased the changes of rCBF in rats. The rCBF of Nelumbo nucifera was not changed by pretreated propranolol, atropine, L-NNA and indomethacin. But the rCBF of Nelumbo nucifera was decreased by pretreated methylene blue. Nelumbo nucifera decreased the BP significantly. The BP of Nelumbo nucifera was not changed by pretreated propranolol, atropine, L-NNA and indomethacin. But the BP of Nelumbo nucifera was decreased by pretreated methylene blue. These results indicated that Nelumbo nucifera might increase the rCBF and decrease the BP which related to guanylyl cyclase activity.

• Journal of Chest Surgery
• /
• 제20권3호
• /
• pp.610-618
• /
• 1987

A 23-y-o male patient was suffered from intermittent fainting and dyspnea on exertion [NYHA Class IIIIV]. 2-D - Echocardiogram and cardiac catheterization with cineangiogram showed typical IHSS findings those were asymmetrical septal hypertrophy [ASH], systolic anterior motion of anterior mitral leaflet [SAM] which induced mild mitral regurgitation [Seller Grade I/IV] and pressure gradient about 60 mmHg between left ventricle and the aorta. Medical treatment with 8-adrenergic blockade [propranolol] and Ca" channel antagonist [Verapamil] had no response. So, we performed trans-aortic ventricular septal myotomy and mymectomy. Resected rectangular muscle bar was 1 Cm x 1 Cm x 4.5 Cm. Post-operative pressure gradient between the left ventricle and the aorta was less than 10 mmHg and SAM. was disappeared with decreased mitral regurgitation grade. Post-operative course was smooth and his symptoms and signs were free without any medication during 12 months follow-up.w-up.

• Journal of Microbiology and Biotechnology
• /
• 제14권6호
• /
• pp.1338-1342
• /
• 2004

Cyclosophoraoses (Cys), cyclic ${\beta}-(1{\rightarrow}2)-D-glucans$ produced by Rhizobium meliloti 2011, were used as a novel chiral stationary phase for the enantiomeric separation. A novel Cys stationary phase, chemically immobilized onto porous silica via aminopropyltrimethoxysilane as a molecular linker, showed good separation for each racemate of bupivacain (separation factor, $\alpha$=1.3), propranolol ($\alpha$=1.3), and fenoprofen ($\alpha$=2.9), respectively, under the mobile phase of water: methanol (80:20, v/v) at a constant flow rate of 0.9 ml/min at pH7.

• Journal of Ginseng Research
• /
• 제22권3호
• /
• pp.200-205
• /
• 1998

Isolated rabbit jejunal segments were used to study the effects of ginseng total saponins (GTS) , protopanaxatriol saponins (PT) and protopanaxadiol saponins (PD) on intestinal contractility. GTS, PT and PD caused a dose-dependent decrease in intestinal spontaneous movements, and PT was the most efficacious of them. The effect of GTS, PT and PD were not blocked by pretreatment with phentolamine (10-6 M), yohimbine (10-6 M), d1-propranolol (10-6 M), naloxone(10-6∼10-5M), Nu-nitro-L-arginine methyl ester (10-4 M), methylene blue (10-5M), and N-ethylmaleimide (10-4 M). However, pretreatment with tetraethylammonium chloride (3-10 mM) antagonized the effect of GTS, PT and PD. Furthermore, 4-amlnopyridine (1 mM) also inhibited the effect of GTS, PT and PD. The results suggest that GTS, PT and PD inhibited the spontaneous movements in isolated rebait jejunum by causing hyperpolarization through an activation of K+ channels directly.

• 약학회지
• /
• 제24권2호
• /
• pp.101-110
• /
• 1980

희첨(Siegesbeckiae Herba)은 진득찰(Siegesbeckiae pubescens Makino)의 잎을 말하며 한방에서 중풍, 전신마비, 반신불수, 부종등에 사용되어 왔다. 이에 관한 연구로는 한등이 diterpene계의 불합물을 분리하였고 이 diterpene계중의 한 성분이 실험적 신성 고혈압을 유기한 백서에 항고혈압작용이 있음을 보고한바 있으나 이의 고혈압 활료제로의 실용성 여부에 관하여서는 확인된 바가 없어 고혈압 치료제 개발의 일환으로서 화학적 성분 연구에 우선하여 약리학적으로 그 본태를 파악하고저 수성 및 알콜성 엑기스를 축출하여 가토에 대하여 이 실험을 시행하였다.

• 한국식물생명공학회:학술대회논문집
• /
• 한국식물생명공학회 2004년도 생명공학 실용화를 위한 비젼
• /
• pp.74-79
• /
• 2004

Little is known about the effect of epigallocatechin-3 gallate (ESCG), a major constituent of green tea, on the expression of cyclooxygenase (COX)-2. Here, we studied the role of phospholipase D (PLD) isozymes in EGCG-induced COX-2 expression. Stimulation of human astrocytoma cells (U87) with EGCG induced formation of phosphatidylbutanol, a specific product of PLD activity, and synthesis of COX-2protein and its product, prostaglandin $E_2$ ($PGE_2$). Pretreatment of cells with 1-butanol, but not 3-butanol, suppressed EGCG-induced COX-2 expression and $PGE_2$ synthesis. Furthermore, evidence that PLD was involved in EGCG-induced COX-2 expression w3s provided by the observations that COX-2 expression was stimulated by over-expression of PLD1 or PLD2 isozymes and treatment with phosphatidic acid(PA), and that prevention of PA dephosphorylation by 1-propranolol significantly potentiated COX-2expression Induced by EGCG. EGCG induced activation of p38 mitogen-activated protein kinase (p38MAPK), and specific Inhibition of p38 MAPK dramatically abolished EGCG-Induced PLD activation, COX-2 expression, and $PGE_2$ formation. Moreover, protein kinase C (PKC) inhibition suppressed EGCG-induced p38 MAPK activation, COX-2 expression, and $PGE_2$ accumulation. The same pathways as those obtained in the astrocytoma cells were active in primary rat astrocytes, suggesting the relevance of the findings. Collectively, our results demonstrate for the first time that PLD isozymes mediate EGCG-induced COX-2 expression through PKC and p38 in immortalized astroglial line and normal astrocyte cells.

• Archives of Pharmacal Research
• /
• 제25권5호
• /
• pp.675-680
• /
• 2002

In order to investigate the underlying mechanism of HCI in oesophagitis, the inflammatory response to HCI was observed in RBL-2H3 mast cells. Rat basophilic leukemia (RBL-2H3) cells were used to measure histamine release, arachidonic acid (AA) release, reactive oxygen species (ROS) and peroxynitrite generation induced by HCI. Exogenous HCl increased the level of histamine release and ROS generation in a dose dependent manner, whereas it decreased the spontaneous release of [$^3$H] M and the spontaneous production of peroxynitrite. Mepacrine (10 $\mu$M), oleyloxyethyl phosphorylcholine (10 $\mu$M) and bromoenol lactone (10 $\mu$M) did not affect both the level of histamine release and ROS generation induced by HCI. U73122 (1 $\mu$M), a specific phospholipase C (PLC) inhibitor did not have any influence on level of histamine release and ROS generation. Propranolol (200 $\mu$M), a phospholipase D (PLD) inhibitor, and neomycin (1 mM), a nonspecific PLC and PLD inhibitor, significantly inhibited both histamine release and ROS generation. Diphenyleneiodonium (10 $\mu$M), a NADPH oxidase inhibitor, and tiron (5 mM), an intracellular ROS scavenger significantly inhibited the HCI-induced histamine release and ROS generation. These findings suggest that the inflammatory responses to HCI is related to histamine release and ROS generation, and that the ROS generation by HCI may be involved in histamine release via the PLD pathway in RBL-2H3 cells.

• 수면정신생리
• /
• 제18권1호
• /
• pp.40-44
• /
• 2011

기면병은 과도한 주간 졸림, 탈력발작, 수면 분절화, 입면환각의 특징을 가진 수면 질환이다. 기면병의 증상은 내과적, 신경과적 질환으로부터 생길 수도 있다. 17세의 고등학생 남자 환자가 3개월 전부터 발생한 참을 수 없는 과도한 주간 졸림으로 본원 수면클리닉을 통해 입원하였다. 내원 이후 측정된 체질량지수는 30.4 kg/$m^2$였고 맥박은 분당 70~90회, 혈압은 150/100~120/70 mmHg로 관찰되었다. 갑상선기능 검사에서 T3 391.2 ng/dL(60~181), free T4 4.38 ng/dL(0.89~1.76), TSH(thyroid stimulating hormone) <0.01 ${\mu}IU$/mL(0.35~5.5)로 갑상선 중독증이 시사되었다. 수면다원검사가 실시되었고, 수면 자세의 변환은 시간당 81 회로 매우 많은 편이었다. 입면 잠복기는 33.5분, 수면 효율은 47.9%, 입면에서 렘수면 입면시간은 153.6분으로 지연되었고 렘수면은 27.1%로 증가하였다. 주기성 사지 운동지수는 13.4/h로 나타났다. 수면잠복기반복검사에서 평균 입면잠복시간은 24초, SOREMP(sleep onset REM period)은 3회에서 관찰되었다. actogram상 수면-각성의 경계가 불분명하였고, HLA typing에서 DQB1 $^*0602$는 음성이었다. 환자의 갑상선중독증은 대해 3개월간 methimazole 30 mg, propranolol 40 mg이 투약되며 갑상선 기능이 호전되었다. 탈력발작은 venlafaxine 75 mg으로 조절되었고, 야간 수면 유지와 주기적 사지운동증을 치료 하기 위해 clonaze-pam 0.5 mg이 사용되었고 주관적인 야간 수면의 질은 향상되었다. 과도한 주간 졸림에 대해서는 3개월간 modafinil 200~400 mg이 투여되었고 부분적이긴 하지만 다소의 호전을 보이고 있다. 본 증례는 기면병으로 최종 진단된 환자에 있어 병력과 검사상 발견된 갑상선 중독증, 그리고 수면 효율 감소 등이 과도한 주간 졸림을 평가하는데 혼란 변수로 작용한 경우라 하겠다. 다만, 주간 과다 졸림이 modafinil에 부분적인 효과를 보이는 것, HLA DQB1 $^*0602$ 음성의 결과를 보인 환자에게 나타났던 탈력발작에 대해서도 더 설명이 필요할 것으로 보인다. 향후 CSF hypocretin level을 추가로 측정하고 수면 문제의 추이를 관찰하면서 추가적인 PSG와 MSLT가 필요할 것으로 사료된다.

• Journal of Yeungnam Medical Science
• /
• 제31권2호
• /
• pp.148-151
• /
• 2014

Radioactive iodine (RAI) therapy is widely used for the treatment of Graves disease. After RAI therapy, 44% become hypothyroid and up to 28% remain hyperthyroid. The development of thyrotoxicosis after RAI therapy is believed to be mediated by 2 different mechanisms: a transient increased release of thyroid hormone due to radiation thyroiditis and the rare development of Graves disease due to the formation of antibodies to the thyroid-associated antigens released from the damaged follicular cells. A 55-year-old woman was hospitalized with severe headache, weight loss, and palpitation. She received a dose of 7 mCi of RAI (I-131) about 6 weeks earlier. Thyroid function test showed 7.98 ng/dL free T4, >8 ng/mL T3, < $0.08{\mu}IU/L$ thyroid stimulating hormone, and high titer thyroid stimulating immunoglobulin (TSI) (85.8 IU/L). She improved with propylthiouracil, propranolol, and steroid treatment. The TSI, however, was persistently elevated for 11 months.