• 식물분류학회지
• /
• 제45권1호
• /
• pp.12-16
• /
• 2015

한국의 십자화과 꽃다지속 식물 우수리꽃다지 (Draba ussuriensis Pohle)를 백두산에서 새로이 발견하여 보고한다. 본종의 특징은 꽃이 흰색이고 다년생인 점이 구름꽃다지(Draba mongolica Turczaninow)와 유사하지만, 줄기와 과경에 털이 없고 경엽의 수가 작은 점이 구름꽃다지와 다르다. 국명은 학명의 종소명에서 유래한 이름을 사용하였다. 또한 과거 백두산 및 관모봉 지역에서 자라는 구름꽃다지는 D. incana L., D. glabella Pursh, D. nipponica Makino, D. daurica DC. 등으로 혼돈하여 알려졌다. 그러나 백두산 및 관모봉에서 채집한 표본들을 조사하고 유연종들과 비교분석한 결과 D. mogolica로 밝혀져 그간 잘못 사용된 학명을 바로 잡았다. 따라서 한국산 꽃다지속 식물은 흰꽃 피는 두 종과, 노란색 꽃이 피는 꽃다지를 포함하여 총 3종이 분포한다.

• 대한전기학회:학술대회논문집
• /
• 대한전기학회 2007년도 제38회 하계학술대회
• /
• pp.410-411
• /
• 2007

In this paper describe for development of conversion program by EMS data acquisition. Currently EMS output data has a arbitrary bus number and incorrect bus name. It is need to delvelop converting program for using this data to analysis real power system. Conversion consist of bus number and bus name convert, machine's MBASE, X''d, Machine ID, Area, Zone Code, adding tie-line and remove small genererator that was not consider in transient stability analysis. As result of this work, the efficiency of power system analysis is increase and the result input data is used for many analysis applications.

• 한국자원식물학회지
• /
• 제21권6호
• /
• pp.427-430
• /
• 2008

Here we reported two unrecorded naturalized species from Korean flora. Andropogon virginicus L. of Graminaeae and Euphorbia postrata Aiton of Euphorbiaceae are collected from Dong-gu, Ulsan-si and Sinjindo-ri, Taean-gun, Chungcheongnam-do respectively. A. virginicus L. was easily distinguishable from Themeda triandras var. japonica Makino by keel on glume, 2-4 racemes and long hairy rachis. Thus, the new Korean name, 'Na-do-sol-sae', was given. E. postrata Aiton was cleary distinguished from related taxa by hairs on only edges of fruits. The new Korean name, 'Nu-un-ttang-bin-dae' was given considering the species epithet. Descriptions, illustrations and photographs showing habitat were given.

• The Korean Journal of Pain
• /
• 제14권1호
• /
• pp.12-18
• /
• 2001

Background: It is controversial whether the change in nitric oxide (NO) expression in the dorsal root ganglia (DRG) may be responsible for developtment and/or maintenance of painful diabetic neuropathy. The aim of this study was to clarify the role of NO in the pathogenesis of painful diabetic neuropathy. Methods: The effect of L-nitroargine methylester (L-NAME) or sodium nitroprusside (SNP) on allodynia was measured in streptozotocin (STZ)-induced diabetic rats. NO concentration was measured in the cerebrospinal fluid (CSF) and plasma of the diabetic rats. NADPH-diaphorase (NADPH-d) histochemistry was performed on the DRG and spinal cords of the STZ-induced diabetic rats. Results: L-NAME, an inhibitor of nitric oxide synthase, alleviated allodynia, while SNP, a nitric oxide donor, aggravated allodynia in diabetic rats. Plasma NO level in the diabetic rats was significantly decreased compared with control rats. NO level in the CSF of diabetic rats did not differ from that of the control rats. NADPH-d positive cells were decreased in the DRG of diabetic rats. However, NADPH-d histochemistry in the diabetic spinal cord was not different from that of the control rats. Conclusions: Downregulation of NO expression in the diabetic rats may not be causally related to the development and/or maintenance of painful diabetic neuropathy.

• 대한수의학회지
• /
• 제45권4호
• /
• pp.485-493
• /
• 2005

We studied the effects of trazodone on arterial blood pressure in anesthesized guinea pigs, and on vascular responses in isolated thoracic aorta. Trazodone produced a concentration-dependent relaxation in phenylephrine-precontracted endothelium intact (+E) rings, but not in a KCl-precontracted aortic rings. These relaxant effects of trazodone on +E rings were significantly greater than those on denuded (-E) rings. The trazodone-induced relaxation was suppressed by glibenclamide and tetrabutylammonium, but not by N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), methylene blue (MB), nifedipine, indomethacin, 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC) and clotrimazole. In vivo, infusion of trazodone elicited a significant decrease in arterial blood pressure. Trazodone-induced blood pressure lowering was markedly inhibited by intravenous pretreatment of prazosin but not by pretreatment of saponin, L-NNA, L-NAME, MB, nifedipine, glibenclamide, clotrimazole and NCDC. In addition, trazodone produced an increase in twitch force of isolated papillary muscle and left ventricular pressure of perfused heart. These findings suggest that the endothelium-independent vasorelaxant effect of trazodone may be explained by activation of $Ca^{2+}$-activated and ATP-sensitive $K^+$ channels, and the hypotensive effect of trazodone is not associated with cardiac contraction.

• 한국동물학회지
• /
• 제36권4호
• /
• pp.556-561
• /
• 1993

Littorophilosa lineuta is described from Korea as new. Four Littorophiloscia species from Japan (L. nipponensis Nunomura, 1986; L. hoyoshii Nunomura, 1986; L. longicouda Nunomura, 1986; L. hvugoensis Nunomura, 1986) are considered to be conspecific. L. nipponensis is chosen as a valid name anti L. koreono Taiti and Ferrara, 1986 from Korea is considered as another junior svnonyrn.

• 대한약리학회지
• /
• 제29권2호
• /
• pp.213-223
• /
• 1993

급성 신성 고혈압쥐 (2-kidney, 1-ligation type)의 전신성 동맥계와 폐 동맥계에 대한 내피 의존적 혈관반응성을 규명하기 위하여, 적출 혈관 및 마취상태의 흰쥐에 대한 acetylcholine (ACh)의 혈관이완작용 및 혈압강하 작용을 측정하였다. 혈장 renin 활성(PRA)은 신동맥 결찰전 $7.31{\pm}0.63\;ng/ml/hr$ A I에 비해 결찰 $6{\sim}8$일후에는 $19{\sim}22\;ng/ml/hr$ A I으로 유의성있게 증가하였으며, 이는 수축기혈압의 상승과 $(154{\pm}1.83{\rightarrow}190{\sim}215\;mmHg)$ 일정한 상관성을 유지하였다. 신성 고혈압쥐 및 정상 혈압쥐의 흉곽 대동맥은 내피세포 존재시 ACh에 의해 용량의존적으로 이완되었으며, 이때 신성고혈압쥐에서의 반응은 정상 혈압쥐에 비해 유의성있게 감소하였다(각각 34% 및 86%, p<0.01). 또한 ACh은 신성 고혈압쥐 및 정상 혈압쥐의 폐동맥에 대해서도 내피세포 존재시에 이완반응을 초래하였다. 그러나, 흉곽 대동맥에서와는 달리 두 군간에 유의성있는 차이가 없었다. 이들 반응은 내피세포 제거후 또는 EDRF 억제제 (L-NAME, MB, $10^{-5}$ M) 투여후 유의성있게 억제되었다. $ACh(0.1{\sim}10\;{\mu}g/kg,\;i.v.)$은 신성 고혈압쥐 및 정상 혈압쥐에서 전신성 동맥압의 강하를 초래하였는데, 신성 고혈압쥐에서 다소 감소하였으나 유의성있는 차이는 없었으며 ($SAPm;\;10\;{\mu}g/kg$에서 각각 39%, 46 %), 이들 작용은 L-NAME(30 mg/kg, i.v.) 전처치후 유의성있게 억제되었다. ACh에 의한 폐동맥압 강하는 신성 고혈압쥐 및 정상 혈압쥐 사이에 서로 비슷하게 나타났다. 그러나, 신성 고혈압 쥐 및 정상 혈압쥐에서 ACh에 의한 폐동맥압의 강하율은 전신성 동맥압의 강하율보다 유의성있게(p<0.01) 작았으며, 또한 L-NAME $(0.1{\sim}100\;mg/kg,\;i.v.)$에 의한 폐동맥압의 상승은 전신성 동맥압의 상승보다 유의성있게(p<0.01) 작았다. 이상의 실험 결과들은 급성 신성 고혈압쥐의 전신성 동맥계에서는 내피세포 손상이 초래되지만, 폐동맥계에서는 초래되지 않는다는것을 제시해준다. 또 신성고혈압쥐 및 정상 혈압쥐에서 EDRF 의 basal release 및 ACh 유발성 EDRF function은 전신성 동맥계에 비해 폐동맥계에서 적다는 것을 제시해준다.

• 한국보건간호학회지
• /
• 제16권1호
• /
• pp.176-189
• /
• 2002

The purpose of this study were to illustrate the various medication error types and causes and identified to related drugs to provide basic data for preventing nurses' medication error by analysing 73 cases of AJN 'medication Error' column(1993, Oct -2000, Nov). Nurses' types of medication error were classified into 7 types. The most frequent error types are wrong medication$(21.9\%)$ and the wrong dose$(21.9\%)$ together. The others are wrong $time(4.1\%)$, $omission(2.7\%)$, mechanical $error(2.7\%)$, incorrect IV $rate(1.4\%)$. wrong route $administration(1.4\%)$ in order. Nurses' causes of medication error were 9 kinds. The most frequent type is confusing between similar drug shape, color, size, name, injection devices and patient's $name(43.9\%)$ and the others are lack of knowledge about $drugs(26.8\%),\; slips(7.3\%),\; miscalculating\;dose(4.9\%)$, incorrect adjusts $devices(4.9\%)$, difficulty to read or illegible decimal $point(4.9\%),$ $abbreviation(2.4\%)$, fatigue with $overwork(2.4\%)$ and no communication with $patient(2.4\%)$ in order. Related drugs with medication error are as follows. - dose unit(IU. minims. mcg/min. mEq) : Heparin. insulin. synthetic calcitonin, some enzymes and hormones, vitamins, some antibiotics, tuberculin injection. MgSO4 injection. nitroglycerin - similar size, color and shape drug : $0.9\%$ N/S and acetic acid $0.25\%$ for irrigation. premixed 2mg lidocaine sol. and $0.9\%$ N/S, gentamycin 20mg/2mL for children and 80mg/2mL for adult, dextroamphetamine 5mg and 10mg capsule. sedatives chloral hydrate 250mg/5mL and 500mg/5mL - similar name :Aredia(pamidronate disodium) and Adriamycin(doxorubicin), Lamictal (lamotrigine) and Lamisil 250mg. Elderpryl and enalapril, cefotaxime and cefoxitin, carboplatin and cisplatin, sumatriptan and zolmitriptan, Celebrex and Celexa, Humulin and Humalog, Percodan and Percocet, Diabeta and Diabinese, Epivir and Retrovir, Xanax(alprazolam) and Zantac(ranitidine) - decimal point : low molecular weight warfarin, methotrexate - unfamiliar drug uses of familiar drug ; methotrexate. droperidol, imipramine, propranolol - number of drug name(misleading chemical name) : 6-thioguanine, 6-mercaptopurine, 5-fluorouracil - type of administration route : Oxycodone(OxyContin). - administration time : acarbose(Precose). - injection way (Z-track method): hydroxyzine - epidural cathether : LMWHs(enoxaparin, dalteparin), - ADD Vantage self contained delivery system : ceftriaxone(Rocephin)

• 대한수의학회지
• /
• 제44권4호
• /
• pp.515-522
• /
• 2004

The vasorelaxant effect of serotonin reuptake inhibitor fluoxetine was investigated in rat isolated thoracic aorta. Fluoxetine induced a concentration-dependent relaxation in aorta precontracted with phenylephrine (PE) and KCl. These relaxations were suppressed by removal of the endothelium (-E) or pretreatment of nitric oxide synthase inhibitors, N(G)-nitro-L-arginine (L-NNA) and N(omega)-nitro-Larginine methyl ester (L-NAME), guanylate cyclase inhibitors, methylene blue (MB) and 1H-[1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one (ODQ), and $Ca^{2+}$ channel blockers, nifedipine and verapamil, in PE-precontracted +E rings. However, fluoxetine-induced relaxations were not suppressed by pretreatment of $K^{+}$ channel blockers, tetrabutylammonium and glibenclamide, in PE-precontracted endothelium intact (+E) rings. The fluoxetine-induced relaxations were not suppressed by removal of the endothelium or pretreatment of LNNA and MB in KCl-precontracted +E rings. Also, fluoxetine inhibited PE-induced sustained contraction in +E rings. These inhibitory effects of fluoxetine on contractions could be reversed by removal of the endothelium or pretreatment of L-NNA, L-NAME, MB, ODQ, nifedipine and verapamil, but not by pretreatment of etrabutylammonium and glibenclamide. These findings suggest that the vasorelaxant effect of fluoxetine is modulated by intracellular $Ca^{2+}$ with an involvement of endothelial NO-cGMP pathway and also may be related to the inhibition of $Ca^{2+}$ entry through voltage-gated channel.

• The Korean Journal of Pain
• /
• 제35권4호
• /
• pp.413-422
• /
• 2022

Background: The neocortex, including the medial prefrontal cortex (mPFC), contains many neurons expressing nitric oxide synthase (NOS). In addition, increasing evidence shows that the nitric oxide (NO) and opioid systems interact in the brain. However, there have been no studies on the interaction of the opioid and NO systems in the mPFC. The objective of this study was to investigate the effects of administrating L-arginine (L-Arg, a precursor of NO) and N(gamma)-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NOS) into the mPFC for neuropathic pain in rats. Also, we used selective opioid receptor antagonists to clarify the possible participation of the opioid mechanism. Methods: Complete transection of the peroneal and tibial branches of the sciatic nerve was applied to induce neuropathic pain, and seven days later, the mPFC was cannulated bilaterally. The paw withdrawal threshold fifty percent (50% PWT) was recorded on the 14th day. Results: Microinjection of L-Arg (2.87, 11.5 and 45.92 nmol per 0.25 µL) increased 50% PWT. L-NAME (17.15 nmol per 0.25 µL) and naloxonazine (an antagonist of mu opioid receptors, 1.54 nmol per 0.25 µL) inhibited anti-allodynia induced by L-Arg (45.92 nmol per 0.25 µL). Naltrindole (a delta opioid receptor antagonist, 2.45 nmol per 0.25 µL) and nor-binaltorphimine (a kappa opioid receptor antagonist, 1.36 nmol per 0.25 µL) were unable to prevent L-Arg (45.92 nmol per 0.25 µL)-induced antiallodynia. Conclusions: Our results indicate that the NO system in the mPFC regulates neuropathic pain. Mu opioid receptors of this area might participate in pain relief caused by L-Arg.