Repellent Effect of Camomile and Lavender Essential Oils against House Dust Mite in Bed Fabric

Myun-Goo Kang,지차호 충북대학교 동물의학연구소 2012 Journal of Biomedical and Translational Research Vol.13 No.1

House dust mite (HDM) allergens has been associated with allergic disease such as asthma, allergic rhinitis and atopic dermatitis. In order to control of house dust mites, various acaricidal agents have been suggested but their remains act as allergens even after death. Therefore, expelling the mite is more effective policy than killing them because of avoidance of allergen. In this experiment, we compared the repellent effect of two essensial oils (Matricaria chamomilla, Lavandula vera) against house dust mites, Dermatophagoids farinae and D. pteronyssinus in bed fabric. The essential oils were applied by direct contact method at various doses (0.1, 0.05, 0.025, 0.0125, 0.00625 μl/cm2) and at a various exposure times (30, 60, 120, 180, 240 min). The result of this experiment suggests two oils have a significant repellent activity. Camomile essential oil in 0.0125 μl/cm2 at 240 minutes caused 93.7% repellent effect and lavender essential oil in 0.05 μl/cm2 at 180 minutes caused 88.9% of repellent effect. The result show that camomile essential oil has more potent repellent activity than lavender essential oil in particular concentration.

Repellent Effect of Camomile and Lavender Essential Oils against House Dust Mite in Bed Fabric

Cha-Ho Jee, Myun-Goo Kang 충북대학교 동물의학연구소 2012 Journal of Biomedical and Translational Research Vol.13 No.1

House dust mite (HDM) allergens have been associated with allergic diseases, such as asthma, allergic rhinitis, and atopic dermatitis. Various acaricidal agents have been suggested for control of house dust mites; however, their remains act as allergens even after death. Therefore, for avoidance of allergen, expelling the mites is a more effective policy than killing them. In this experiment, we compared the repellent effect of two essential oils (Matricaria chamomilla, Lavandula vera) against house dust mites, Dermatophagoids farinae and D. pteronyssinus in bed fabric. The essential oils were applied by direct contact method at various doses (0.1, 0.05, 0.025, 0.0125, and 0.00625 μl/cm2) and at various exposure times (30, 60, 120, 180, and 240 min). Results of this experiment suggest that the two oils have significant repellent activity. Camomile essential oil in 0.0125 μl/cm2 at 240 minutes had a repellent effect of 93.7% and lavender essential oil in 0.05 μl/cm2 at 180 minutes had a repellent effect of 88.9%. The results of this study showed that camomile essential oil has more potent repellent activity than lavender essential oil at a particular concentration.

저산소성 폐질환에서 폐동맥압의 비관혈적 측정에 관한 연구

이진구(Jin Goo Lee),인광호(Kwang Ho In),박상면(Sang Myun Park),조재연(Jae Yeon Jho),심재정(Jae Jeong Shim),강경호(Kyung Ho Kang),심완주(Wan Joo Shim),유세화(Se Hwa Yoo) 대한내과학회 1995 대한내과학회지 Vol.49 No.4

Objectives: The presence of pulmonary hypertension in patients with hypoxic lung disease is associated with poor prognosis. Right heart catheterization is the reference method for the diagnosis of pulmonary arterial hypertension but this invasive technique is not always well tolerated in all patients with hypoxic lung disease. There is a need for noninvasive method to allow the accurate estimation of pulmonary arterial pressure in these patients. To find reliable noninvasive methods of measuring pulmonary artery pressure, we evaluated the reliability of continuous wave Doppler echocardiography and gated cardiac blood pool scintigraphy in patents with hypoxic lung disease. Methods: Noninvasive measurements of systolic pulmonary artery pressure by continuous wave Doppler echocardiography and right ventricular ejection fraction by gated cardiac blood pool scintigraphy were compared with systolic pulmonary atery pressure measured by cardiac catheterization in 12 patients with hypoxic lung disease. Results: 1) The systolic pulmonary artery pressures estimated by continuous wave Doppler echocardiography correlated closely with those measured by cardiac catheterization (r=0.88, p<0.01) 2) The right ventricular ejection fraction estimated by gated cardiac blood pool scintigraphy was also correlated well with the systolic pulmonary artery pressure measured by cardiac catheterization (r=0.85, p<0.01). Conclusion: Continuous wave Doppler echocar-diographic estimation of systolic pulmonary artery pressure and gated car diac blood pool scintigraphic estimation of right ventricular ejection pressure are reliable and feasible noninvasive assessment of pulmonary hypertension in patients with hypoxic lung disease.

췌장염 증상없이 췌장-흉막루를 통해 발생한 흉막저류

박상면 ( Sang Myun Park ),이상화 ( Sang Hwa Lee ),이진구 ( Jin Goo Lee ),조재연 ( Jae Youn Cho ),심재정 ( Jae Jeong Shim ),인광호 ( Kwang Ho In ),강경호 ( Kyung Ho Kang ),유세화 ( Se Hwa Yoo ) 대한결핵 및 호흡기학회 1995 Tuberculosis and Respiratory Diseases Vol.42 No.2

만성 호중구성 백혈병(Chronic Neutrophilic Leukemia) 1예

정재면,홍택원,고동희,강준구,김태종,이웅수,최정혜,안명주,김인순,최일영,이영열 한양대학교 의과대학 2002 한양의대 학술지 Vol.22 No.2

Chronic neutrophilic leukemia is a very rare myeloproliferative disorder characterized by splenomagaly, persistent neutrophilia, bone marrow granulocyte hyperplasia, elevated leukocyte alkaline phosphatase, the absense of philadelphis cheomosome. Recently we have experienced a case of chronic neutrophilic leukemia in a 73 years old woman who complained of general weakness. On admission, peripheral blood examination showed leukocytosis with mature neutrophil: Hb 10.5g/㎗, WBC 33,200/㎣, platelet 751,000/㎣ and neutrophoil 93% in differential count. The underlying disease for leukemoid reaction has not been detected. Leukocyte alkaline phospatase score was elevated. Bone marrow study revealed hypercellular marrow with prominent neutrophilic hyperplasia and without myelofibrosis. The cytogenic study shows normal bone marrow cell karyotype without philadephia chromosome.

Role of cysteinyl leukotriene signaling in a mouse model of noise-induced cochlear injury

Park, Jung-Sub,Kang, Seo-Jun,Seo, Mi-kyoung,Jou, Ilo,Woo, Hyun Goo,Park, Sang Myun National Academy of Sciences 2014 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.111 No.27

<P>Noise-induced hearing loss is one of the most common types of sensorineural hearing loss. In this study, we examined the expression and localization of leukotriene receptors and their respective changes in the cochlea after hazardous noise exposure. We found that the expression of cysteinyl leukotriene type 1 receptor (CysLTR1) was increased until 3 d after noise exposure and enhanced CysLTR1 expression was mainly observed in the spiral ligament and the organ of Corti. Expression of 5-lipoxygenase was increased similar to that of CysLTR1, and there was an accompanying elevation of CysLT concentration. Posttreatment with leukotriene receptor antagonist (LTRA), montelukast, for 4 consecutive days after noise exposure significantly decreased the permanent threshold shift and also reduced the hair cell death in the cochlea. Using RNA-sequencing, we found that the expression of matrix metalloproteinase-3 (MMP-3) was up-regulated after noise exposure, and it was significantly inhibited by montelukast. Posttreatment with a MMP-3 inhibitor also protected the hair cells and reduced the permanent threshold shift. These findings suggest that acoustic injury up-regulated CysLT signaling in the cochlea and cochlear injury could be attenuated by LTRA through regulation of MMP-3 expression. This study provides mechanistic insights into the role of CysLTs signaling in noise-induced hearing loss and the therapeutic benefit of LTRA.</P>

산화질소 ( Nitric Oxide ) 의 기도내 신경성 염증 조절에 관한 연구

심재정(Jae Jeong Shim),박상면(Sang Myun Park),이진구(Jin Goo Lee),조재연(Jae Yeun Cho),인광호(Kwang Ho In),유세화(Se Hwa Yoo),강경호(Kyung Ho Kang),김철환(Chul Hwan Kim) 대한내과학회 1994 대한내과학회지 Vol.47 No.4

Baekground: Asthma is classified as an inflammatory disease because there are inflammatory changes in the asthmatic airways. There are many evidences that sensory neuropeptides are involved in these inflammatory responses. Neurogenic inflammation is caused by the antidromic nonadrenergic noncholinergic (NANC) release of neuropeptides from vagal nerves. Recently nitric oxide (NO) has received considerable attention as a messenger molecule in the peripheral nervous system and relaxes airway smooth muscle. Also NO is a potent vasodilator and involved in plasma exudation from airway vessels, To investigate the role of nitric oxide in neurogenic inflammation, neurogenic inflammatory responses in rat airways according to duration of NANC stimuation and effects of NO were evaluated, Method: Neurogenic inflammation was produced in rat airways of 2 experimental groups of 1 min and 2 min stimulation with 5V, 1mSec, 5Hz after cholinergic and adrenergic blockade and compared with sham NANC, The magnitude of airway microvascular leakages was checked in the trachea, main bronchus, peripheral bronchus, and lung parenchyme and the leakeage was measured by Evans blue dye extravasation. NW-nitro-L-arginine (L-NNA, 5 mg/kg iv), L-NNA and L-arginine (50 mg/kg iv) were given 15 min before 2 min stimulation on 3 separate groups for evaluation of NO effects, and microvascular leakage was compared with 2 min NANC stimulation group. Results: 1) Vascular permeability of 1 min NANC stimulation group was increased trachea (208.2%, p<0.05), main bronchus (169.4%, p<0.05), and peripheral bronchus (123.6, p=0.18) compared with sham NANC group. 2) There was about l.5 times increase of vascular permeability in 2 min stimulation group compared with 1 min stimulation group (p<0,05), but not significantly increased permeability of lung parenchyme in both groups. 3) In L-NNA pretreated stimulation oup, there was increased vascular permeability of the trachea (133.3%, p<0.05), main bronchus (167.4%, p<0.05), and peripheral bronchus (197.1%, p<0.05) compared with 2 min stimulation group. 4) L-NNA and L-arginine pretreated stimulation group revealed suppressed vascular permeability com- pared with L-NNA pretreated stimulation group. Conclusion: These results revealed that neurogenic inflammation in the rat airway increases inflammatory responses according to duration of stimulation and blocking of NO synthetase increases neurogenic inflammation. These results provide that nitric oxide modulates inflammatory response of NANC stimulation of the vagal nerves in the rat airways.

실험견의 급성 저산소성 폐고혈압증에서 K+ Channel 의 역할

조재연(Jae Youn Cho),박상면(Sang Myun Park),박희남(Hee Nam Park),이진구(Jin Goo Lee),심재정(Jae Jeong Shim),인광호(Kwang Ho In),강경호(Kyung Ho Kang),유세화(Se Hwa Yoo) 대한내과학회 1996 대한내과학회지 Vol.50 No.3

Objectives: Numerous studies about mediators in acute hypoxic process have been done. These studies revealed that endothelium derived relaxing factor(EDRF, known as nitric oxide) contributed greatly to the pathogenesis of hypoxic pulmonary hypertension and endothelium derived hyperpolarizing factor(EDHF) regulated the tone of vascular smooth muscle. EDHE is known to open K+ channel, hyperpolarizes vascular smooth muscle cells, closes voltage-dependent Ca++ channel and finally relaxes vascular smooth muscle. Some studies revealed that acute hypoxic pulmonary hypertension was developed by inhibition of EDRF &EDHF. To investigate the role of K+ channel in pulmonary hypertension during acute hypoxia, we measured changes of hemodynamic parameters in experimental dogs after adding glibenclamide(K+ channel blocker), methylene blue(S-guanylate cyclase inhibitor), L-NNA(NO synthase inhibitor) and nicorandil(K+ channel opener and S-guanylate cyclase activator). Methods: Six dogs were anesthetized with thiopental sodium and mechanically ventilated with Harvard volume-cycled animal ventilator. Venous and arterial catheters were placed in the limb vein for infusion and femora} artery to measure systemic arterial pressure. Swan-Ganz catheter was inserted via right internal jugular vein for measuring pulmonary arterial pressure, pulmonary capillary wedge pressure asnd cardiac output. We measured the influence of glibenclamide (3mg/kg). methylene blue(lmg/kg), L-NNA (30mg/kg) and nicorandil(300μg/kg) on the changes of hemodynamic parameters during normoxia and hypoxia. Results: The infusion of nicorandil did not affect mean pulmonary arterial pressure during normoxia and significantly inhibited the increase of mean pulmonary arterial pressure during hypoxia. Glibenclamide did not change mean pulmonary arterial pressure during normoxia, but significantly augmented the increase of mean pulmonary arterial pressure during hypoxia. Methylene blue infusion did not affect mean pulmonary arterial pressure during normoxia, but moderately augmented the increase of mean pulmonary arterial pressure during hypoxia. The infusion of L-NNA did not affect mean pulmonary arterial pressure during normoxia and augmented the increase of mean pulmonary arterial pressure singnificantly during hypoxia, The increase of pulmonary arterial pressure induced by glibenclamide, methylene blue, and L-NNA, under hypoxic state was inhibited by nicorandil. Conclusion: Glibenclamide (K channel blocker) did not affect the mean pulmonary arterial pressure in normoxic state, but augmented the pulmonary hypertension during hypoxia and this effect was inhibited by nicorandil. It is suggested that K+ channel contributes to pulmonary hypertension developed during hypoxia, and the depressive effect of nicorandil seems to be attributable to its dual actions as a K' channel opener and an activator of S-guanylate cyclase.

항림프구 글로불린의 조혈작용 기전에 대한 연구

조경란,김태엽,강준구,홍택원,백상현,정재면,박준성,김동욱,신성준,최찬범,최정혜,안명주,김인순,최일영,김병국,김은실,이영열 한양대학교 의과대학 2002 한양의대 학술지 Vol.22 No.2

배경: 재생불량성빈혈 치료 중 하나인 항림프구 글로블린(ALG)/항흉선세포 글로블린은 조혈세포의 자극에 의한 조혈세포 성장인자의 분비 때문일 것이라는 연구가 최근 보고되고 있어 생체 외에서 ALG의 조혈과정에 미치는 영향을 규명하고자 하였다. 방법: 말초혈액 단핵구는 정상인의 말초혈액을 Ficoll-Hypaque에 의해 분리한 후 단구는 2회 연속 부착법으로, T 림프구는 양적혈구를 이용하여 분리하였고 이 순수도는 flow cytometer에 의해 95% 이상임을 확인하였다. 분리된 각 세포는 conditioned medium으로 처리한 후 thymidine uptake test로 세포 증식을 관찰하였고 조혈세포 생체 외 배양은 methylcellulose를 이용한 반고형 배지법을 사용하였다. 결과: 말초혈액 단핵구에 대해 ALG 농도 50μg/mL사이에서 증식을 관찰할 수 있었으며 최대의 효과를 나타낸 농도는 250μg/mL였다. T 림프구 단독 혹은 T 림프구와 단구에서도 ALG 농도 50μg/mL에서 500μg/mL사이에서 효과를 관찰할 수 있었으며 최대효과를 나탸낸 농도는 250μg/mL였다. 그러나 이들 세포군에서는 말초혈액 단핵구보다는 낮은 cpm 값을나타냈고 T 림프구보다는 T+ 단구의 경우에서 더 높은 값을 보여 주었다. 단구만을 대상으로 실험한 경우에서는 모든 ALG 농도에서 세포 내로의 methyltritiated thymidine의 incoporation을 관찰할 수 없었다. ALG-stimulated T lymphocyte-conditioned medium에서는 생체 외 배양에서 얻어진 colony (CFU-GM)가 154개로서 대조군으로 삼은 PHA-LCM의 경우보다 훨씬 많이 형성되었고 ALG-stimulated monocyte-conditioned midium으로 세포배양을 했을 때는 CFU-GM이 64개로 phytohemagglutinin-stimulated leucocyte-conditioned midium의 79개보다는 적지만 12시간 혹은 3일간 세포없이 ALG만으로 배양한 conditionde midium인 12h ALG-M, 3d ALG-M이나 ALG없이 Isocove's modified Dulbecco's medium과 세포만으로 배양한 경우(ALG-0)보다는 많이 관찰되었다. 결론: 본 연구에서 ALG가 정상인에서 면역 자극효과가 있고 혼합배양에서 더 큰 증식효과가 발견되어 둘 사이에 상승효과가 있음을 발견하였다. 생체 외에서 과립구생성(granulopoiesis)을 조절하는 조혈인자의 생성에는 T림프구와 단구의 복잡한 상호작용에 의해 조절되고 항림프구 글로불린으로 자극받은 단구에서 조혈형성인자의 분비됨을 알 수 있었다. 이로서 재생불량성빈혈 환자에서 항림프구 글로블린으로 치료하기 전 생체 외 검사를 시행함으로서 임상 반응을 관찰하는 데 도움이 되리라 생각된다. Background/Aims: Several studies revealed that the antilymphocyte globulin(ALG) / antithymocyte globulin had immunostimulatory effect on hematopoiesis. The aim of this study was to evaluate how the ALG act on the hematopoiesis. Methods: Peripheral blood mononuclear cell (PBMNC) was isolated from normal human blood by Ficoll-Hypaque, monocyte from PBMNC by 2 sequential adherence method and T lymphocyte from sheep RBC. Thier purity was all above 95% by flow cytometer. The clones isolated from each cells were cultured in conditioned midium, observed by thymidine uptake test. The cultures of hematopoietic cells, in vitro were obtained using methylcellulose media. Results: The clones of PBMNC, T lymphocyte and monocyte all started to proliferate at ALG conc. 50μg/mL with their peak at ALG conc.250μh/mL. The proliferation was achieved at a greater degree in a T lymphocyte and monocyte mixture than when done separately in ALG conc.250μg/mL. The clones from ALG-stimulated T lymphocyte- conditioned medium or ALG-stimulated monocyte-conditioned medium proliferated more than in a medium without these stimulatory cells. Conclusion: We found that ALG had immunostimulatory effect on hematopoiesis, with its effect potentiated by interaction with T lymphocyte and monocyte, which could be controlled, in vitro.

MRP1 Polymorphisms Associated With Citalopram Response in Patients With Major Depression

Lee, Sung Hee,Lee, Min-Soo,Lee, Ji Hyun,Kim, So Won,Kang, Rhee-Hun,Choi, Myoung-Jin,Park, Sang Jin,Kim, Se Joo,Lee, Jae Myun,Cole, Susan P.C.,Lee, Min Goo Lippincott Williams Wilkins, Inc. 2010 JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY Vol.30 No.2

Multidrug resistance protein 1 (MRP1, ABCC1) transports antidepressive agents in the endothelial cells of the blood-brain barrier. Therefore, polymorphisms in the MRP1 gene may affect the treatment response of antidepressants. This study was aimed to identify the association between genetic variations in MRP1/ABCC1 and the therapeutic response to the antidepressant citalopram. One hundred and twenty-three patients who had been treated with citalopram monotherapy to control their major depressive disorder were recruited, and genotype data from 64 patients who had completed their 8-week follow-up were evaluated together with those from 100 controls. Nine MRP1 single nucleotide polymorphisms (SNPs) showing more than 5% allele frequency in the Korean population were analyzed. The c.4002G>A, a synonymous SNP in exon 28, showed a strong association with the remission state at 8 weeks (P = 0.005, odds ratio [OR], 4.7, 95% confidence interval [CI], 1.5∼14.7). The c.4002G>A forms a linkage disequilibrium block with 3 other SNPs including c.5462T>A in the 3' untranslated region. Accordingly, the haplotype showed a significant association with the remission state (P = 0.014). Subsequent molecular studies also supported the association between these MRP1 polymorphisms and the citalopram response. Thus, kinetic studies using MRP1-enriched membrane vesicles revealed that citalopram is a substrate of MRP1 (Km = 1.99 μM, Vmax = 137 pmol/min per milligram protein). In addition, individuals with c.4002G>A or c.5462T>A polymorphisms showed higher MRP1 mRNA levels in peripheral blood cells. These results suggest that MRP1 polymorphisms may be a predictive marker of citalopram treatment in major depression.