난포기 및 황체기에 있어서 돼지 난관 협부 평활근의 neurotransmitter들의 수축효과에 대한 estradiol-17β및 progesterone의 영향

이민기,노규진,심철수,남윤정,김주현,최상용 慶尙大學校 1991 論文集 Vol.30 No.2

The effects of estradiol-17β or progesterone on the contractility of neurotransmitters on pig oviductal isthmic smooth muscle were investigated. The motility of the isolated smooth muscle was recorded by using physiological recording system. The results were summarized as follows : 1. The contractility induced by histamine or prostaglandin F2α was depressed by the pretreatment of estradiol-17β but was not by the preteatment of progesterone in follicular or luteal stage. 2. The contractility induced by acetylcholine was depressed un follicular stage but excited in luteal stage by the pretreatment of estradiol-17β or progesterone. 3. The contractility induced by norepinephrine was depressed by the pretreatment of progesterone in follicular stage but was excited by the pretreatment estradiol-17β in luteal stage.

Fe₃S₄/Fe₇S₈-promoted degradation of phenol via heterogeneous, catalytic H₂O₂ scission mediated by S-modified surface Fe²⁺ species

Choe, Yun Jeong,Byun, Ji Young,Kim, Sang Hoon,Kim, Jongsik Elsevier 2018 Applied catalysis. B, Environmental Vol.233 No.-

<P><B>Abstract</B></P> <P>Enhancing OH productivity via heterogeneous, catalytic H<SUB>2</SUB>O<SUB>2</SUB> activation is a long-standing conundrum in H<SUB>2</SUB>O purification and thus requires the renovation of conventional reaction systems. The initial step in realizing advanced H<SUB>2</SUB>O<SUB>2</SUB> decomposition via heterogeneous catalytic manner is the exploration of the solid capable of efficiently cleaving OO bond inherent to H<SUB>2</SUB>O<SUB>2</SUB> and minimizing the loss of catalytic species during vigorous reaction dynamics. While using phenol as a model compound for recalcitrants, this paper highlights the use of Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> as a catalyst to enhance OH productivity and thus promote phenol degradation via electro-Fenton reaction over conventional Fe<SUB>2</SUB>O<SUB>3</SUB>, Fe<SUB>3</SUB>O<SUB>4</SUB>, and other sulfide analogue (FeS<SUB>2</SUB>). Materials’ characterizations and kinetic interpretation of reaction runs under controlled environments served to substantiate the benefits which were provided by Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> during the reaction. Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> incorporated greater amount of S-modified, surface-exposed Fe<SUP>2+</SUP> sites to cleave H<SUB>2</SUB>O<SUB>2</SUB> than FeS<SUB>2</SUB>. This improved catalytic consequence of Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> (i.e., phenol conversion and initial reaction rate), as also evidenced by control runs detailing H<SUB>2</SUB>O<SUB>2</SUB> decomposition in conjunction with <I>tert</I>-butyl alcohol-driven OH scavenging. Filtration control runs as well as recycle runs were also used to verify that Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> could heterogeneously catalyze H<SUB>2</SUB>O<SUB>2</SUB> scission under the mild, adequate reaction environments, which were realized by the use of low electrical powers and the catalyst immobilized on a cathode.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> with greater amount of surface Fe<SUP>2+</SUP> species to dissociate H<SUB>2</SUB>O<SUB>2</SUB> compared to FeS<SUB>2</SUB>. </LI> <LI> Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> with supported Fe<SUP>2+</SUP> sites to heterogeneously catalyze H<SUB>2</SUB>O<SUB>2</SUB> fragment. </LI> <LI> Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> with promoted catalytic H<SUB>2</SUB>O<SUB>2</SUB> scission ability compared to Fe<SUB>2</SUB>O<SUB>3</SUB>, Fe<SUB>3</SUB>O<SUB>4</SUB>, and FeS<SUB>2</SUB>. </LI> <LI> Fe<SUB>3</SUB>S<SUB>4</SUB>/Fe<SUB>7</SUB>S<SUB>8</SUB> with enhanced phenol degradation performance over other Fe-analogues. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Anthocyanins in the black soybean (Glycine max L.) protect U2OS cells from apoptosis by inducing autophagy via the activation of adenosyl monophosphate-dependent protein kinase

CHOE, YUN-JEONG,HA, TAE JOUNG,KO, KYOUNG-WON,LEE, SUN-YOUNG,SHIN, SEOK JOON,KIM, HO-SHIK Spandidos Publications 2012 ONCOLOGY REPORTS Vol.28 No.6

<P>Anthocyanins (ATCs) have been reported to induce apoptosis in various types of cancer cells, stimulating the development of ATCs as a cancer chemotherapeutic or chemopreventive agent. It was recently reported that ATCs can induce autophagy, however, the mechanism for this remains unclear. In the present report, we carried out mechanistic studies of the mechanism involved in ATC-induced autophagy using ATCs extracted from black soybeans (cv. Cheongja 3, Glycine?max?L.). ATCs clearly induced hallmarks of autophagy, including LC3 puncta formation and the conversion of LC3-I to LC3-II in U2OS human osteosarcoma cells. The induction of autophagy was accompanied by the phosphorylation of multiple protein kinases including extracellular signal-regulated kinase (ERK)1/2, p38 mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK), protein kinase B (AKT) and adenosyl mono-phosphate-dependent protein kinase (AMPK). While chemical inhibitors against ERK1/2, p38 MAPK, JNK and AKT failed to inhibit ATC-induced autophagy, the suppression of AMPK by compound C (CC) as well as siRNA against AMPK reduced ATC-induced autophagy. The treatment of ATCs resulted in a decrease in intracellular ATP contents and the activation of AMPK by AICAR treatment also induced autophagy. It is noteworthy that the reduction of autophagy via the inhibition of AMPK resulted in enhanced apoptosis in ATC-treated cells. In addition, siRNA against forkhead box O3A (FOXO3a), a downstream target of AMPK, suppressed ATC-induced autophagy and p27KIP1 siRNA increased apoptosis in ATC-treated cells. Collectively, it can be concluded that ATCs induce autophagy in U2OS cells via activation of the AMPK-FOXO3a pathway and protect cells from ATC-induced apoptosis via the AMPK-p27KIP1 pathway. These results also suggest that autophagy-modulating agents could contribute to the efficient development of ATCs as anticancer therapy.</P>

Melittin has an inhibitory effect on TNF-α-iduced migration of human aortic smooth muscle cells by blocking the MMP-9 expression

( Yun Jeong Jeong ),( Hyun Ji Cho ),( Key Whang ),( In Seon Lee ),( Kwan Kyu Park ),( Jung Yoon Choe ),( Sang Mi Han ),( Cheorl Ho Kim ),( Hyeun Wook Chang ),( Sung Kwon Moon ),( Wun Jea Kim ),( Yung 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0

Matrix metalloproteinases-9 (MMP-9) plays an important role in the pathogenesis of atherosclerosis and migration of vascular smooth muscle cells (VSMCs) after an arterial injury. In this study, we investigated the potential molecular mechanisms underlying the anti-atheroscleroic effects ofmelittin, a major component of bee venom, in human aortic smooth muscle cells (HASMCs). Melttin significantly suppressed MMP-9 and MMP-2 secretion, as well as TNF-α-induced MMP-9 expression in the HASMCs. In addition, we found that the inhibitory effects of melittin on TNF-α-induced MMP-9 protein expression are associated with the inhibition of MMP-9 transcription levels. Mechanistically, Melittin suppressed TNF-α-induced MMP-9 activity by inhibiting the phosphorylation of p38 and ERK1/2, but did not affect the phosphorylation of JNK and Akt. Reporter gene and western blotting assays showed that melittin inhibits MMP-9 transcriptional activity by blocking the activation of NF-κB via IκBα signaling pathway. Moreover, the matrigel migration assay showed that melittin reduced TNF-α-induced HASMC migration. These results suggest that melittin suppresses TNF-α-induced HASMC migration through the selective inhibition of MMP-9 expression and provide a novel role of melittin in the anti-atherosclerotic action.ⓒ2012Elsevier Ltd. All rights reserved.

Melittin suppresses EGF-induced cell motility and invasion by inhibiting PI3K/Akt/mTOR signaling pathway in breast cancer cells

( Yun Jeong Jeong ),( Yongsoo Choi ),( Jae Moon Shin ),( Hyun Ji Cho ),( Jeong Han Kang ),( Hyeun Wook Park ),( Jung Yoon Choe ),( Young Seuk Bae ),( Sang Mi Han ),( Cheorl Ho Kim ),( Hyeun Wook Chang 영남대학교 약품개발연구소 2014 영남대학교 약품개발연구소 연구업적집 Vol.24 No.0

Bee venom is a natural compound produced by the honey bee (Apis mellifera), and has been reported as having the biological and pharmacological activities, including anti-bacterial, anti-viral and anti-inflammation. In the present study, the inhibitory effects of bee venom and its major peptide components on the tumor invasion were demonstrated. It was confirmed the inhibitory effects of bee venom, melittin, and apamin on the EGF-induced invasion of breast cancer cells. Transwell invasion and wound-healing assays showed that bee venom and melittin significantly inhibits the EGF-induced invasion and migration of breast cancer cells. Also, bee venom and melittin reduced the EGF-stimulated F-actin reorganization at the leading edge, but apamin did not affect. Particularly, melittin inhibited the EGF-induced MMP-9 expression via blocking the NF-κB and PI3K/Akt/mTOR pathway. In addition, melittin significantly suppressed the EGF-induced FAK phosphorylation through inhibition of mTOR/p70S6K/4E-BP1 pathway. These results suggest that inhibitory effects of melittin on breast cancer cell motility and migration may be related to the inhibition of mTOR pathway.ⓒ2014 Elsevier Ltd. All rights reserved.

PGA2-induced HO-1 attenuates G2M arrest by modulating GADD45α expression

Yun-Jeong Choe,고경원,Hyein Lee,이선영,Byung-Chul Kim,Ho-Shik Kim,Ho-Shik Kim 대한독성 유전단백체 학회 2015 Molecular & cellular toxicology Vol.11 No.4

Prostaglandin (PG) A2, a cyclopentenone PG, arrested the growth of U2OS cells in the G2M phase. While inducing G2M arrest, PGA2 increased the expression of heme oxygenase-1 (HO-1) at the level of transcription along with the accumulation of ROS and the activation of MAPKs including JNK, p38MAPK, and ERK1/2. Among the MAPKs, the inhibition of p38MAPK by a specific chemical inhibitor SB203580, or by RNA interference, but not JNK or ERK1/2, attenuated the PGA2-induced transcription of HO-1. Nacetylcysteine (NAC), a ROS scavenger, prevented PGA2-induced G2M arrest, p38MAPK activation and transcriptional induction of HO-1. PGA2 also stimulated GADD45α expression at the level of transcription, and the knockdown of GADD45α repressed PGA2- induced G2M arrest. Finally, the knockdown of the HO-1 protein elevated PGA2-induced GADD45α expression as well as G2M arrest. Collectively, these results suggest that PGA2 causes an increase in ROS accumulation which initiates both HO-1 transcription via p38MAPK, and G2M arrest via GADD45α transcription, and HO-1 attenuates G2M arrest by modulating the expression of GADD45α.

Nutlin-3 induces HO-1 expression by activating JNK in a transcription-independent manner of p53

CHOE, YUN-JEONG,LEE, SUN-YOUNG,KO, KYUNG WON,SHIN, SEOK JOON,KIM, HO-SHIK Spandidos Publications 2014 International journal of oncology Vol.44 No.3

A recent study reported that p53 can induce HO-1 by directly binding to the putative p53 responsive element in the HO-1 promoter. In this study, we report that nutlin-3, a small molecule antagonist of HDM2, induces the transcription of HO-1 in a transcription-independent manner of p53. Nutlin-3 induced HO-1 expression at the level of transcription in human cancer cells such as U2OS and RKO cells. This induction of HO-1 did not occur in SAOS cells in which p53 was mutated and was prevented by knocking down the p53 protein using p53 siRNA transfection, but not by PFT-alpha, an inhibitor of the transcriptional activity of p53. Accompanying HO-1 expression, nutlin-3 stimulated the accumulation of ROS and the phosphorylation of MAPKs such as JNK, p38 MAPK and ERK1/2. Nutlin-3-induced HO-1 expression was suppressed by TEMPO, a ROS scavenger, and chemical inhibitors of JNK and p38 MAPK but not ERK1/2. In addition, nutlin-3-induced phosphorylation of JNK but not p38 MAPK was inhibited by TEMPO. Notably, the levels of nutlin-3-induced ROS were correlated with the mitochondrial translocation of p53 and this induction was prevented by PFT-beta, an inhibitor of the mitochondrial translocation of p53. Consistent with the effect of the ROS scavenger and MAPK inhibitors, PFT-beta reduced HO-1 expression and the phosphorylation of JNK induced by nutlin-3. In the experiments of analyzing cell death, the knockdown of HO-1 augmented nutlin-3-induced apoptosis. Collectively, these results suggest that nutlin-3 induces HO-1 expression via the activation of both JNK which is dependent on ROS generated by p53 translocated to the mitochondria and p38 MAPK which appears to be stimulated by a ROS-independent mechanism, and this HO-1 induction may inhibit nutlin-3-induced apoptosis, constituting a negative feedback loop of p53-induced apoptosis.

요근 농양의 임상적 특징 및 결과 고찰

최정현 ( Choe Jeong Hyeon ),김민철 ( Kim Min Cheol ),임승관 ( Im Seung Gwan ),조숙경 ( Jo Sug Gyeong ),신승수 ( Sin Seung Su ),오윤정 ( O Yun Jeong ),최영화 ( Choe Yeong Hwa ),박광주 ( Park Gwang Ju ),황성철 ( Hwang Seong Cheol 대한내과학회 2003 대한내과학회지 Vol.65 No.3

목적 : 요근 농양은 드물게 발생하는 치명적인 질환으로 비특이적인 임상 양상으로 나타나 진단과 치료가 지연되는 경우가 많다. 이에 저자들은 지난 5년동안 아주대학교 병원에서 진단된 요근 농양 24예의 임상 양상 및 특징, 원인 균주 및 치료 결과에 대해 알아보고자 하였다. 방법 : 1996년 3월부터 2001년 5월까지 아주대학교 병원에서 방사선학적 진단 및 균 배양 검사를 통해 요근 농양으로 진단 후 입원 치료한 24명의 환자를 대상으로 후향적 검토를 Background : Psoas abscess is a rare condition with vague clinical presentations, therefore misdiagnosis or delayed diagnosis is often made. We have reviewed the characteristics of the clinical presentation, microbiology, and treatment of 24 patients with

성인에서 장기간 Furosemide 오용과 연관된 신수질 석회화

최성철 ( Choe Seong Cheol ),김윤구 ( Kim Yun Gu ),김정아 ( Kim Jeong A ),도정호 ( Do Jeong Ho ),한혁준 ( Han Hyeog Jun ),이현희 ( Lee Hyeon Hui ),윤수진 ( Yun Su Jin ),이영기 ( Lee Yeong Gi ),허우성 ( Heo U Seong ),김대중 ( Kim Da 대한신장학회 2001 Kidney Research and Clinical Practice Vol.20 No.6

목 적: Furosemide 장기간 사용은 신생아에서 신수질 석회화(medullary nephrocalcinosis)발생의 주 위험 인자로 알려져 있다. 비록 furosemide가 성인에서도 여러 임상적 상황들에서 사용되지만 성인에서 신수질 석회화와 연관성은 확실하지 않다. 저자들은 성인에서 furosemide 장기간 사용과 신수질 석회화 사이에 연관성이 있는지를 알아보기 위하여 본 연구를 시행하였다. 방 법 : 오랜 기간(복용기간 범위 3-25년) 부종이나 체중 조절을 목적으로 습관적으로 furosemide를 복용한 18명(남 : 녀=1 : 17, 연령범위 21-59세)을 대상으로 하였다. 신수질 석회화는신초음파나 컴퓨터 단층 촬영, 또는 신생검을 통해 확인하였고 대상환자들을 신수질 석회화(+)군과 신수질 석회하(-)군으로 분류하여 임상적 특성들을 비교하였다. 결 과 : 신장 초음파와 컴퓨터 단층 촬영상 신수질 석회화는 양측 신장 수질부 추체(pyramid)들에서 18명 중 15명(83.3%)에서 관찰되었다. Furosemide 오용기간은 신수질 석회화(+)군과 신수질 석회화(-)군에서 차이가 없었지만(10.1±1.7년 대 15.3±0.9, p>0.05), furosemide 하루복용 용량은 신수질 석회화(+)군이 신수질 석회화(-)보다 더 많았다(538±174 대 67±13 mg/일, p<0.01). 두 군간 하루 요 칼슘배설양과 혈청 칼슘, 크레아티닌 청소율치의 차이는 없었다.대상 환자 중 3명에서 시행한 신생검 병리소견에서 국소적인 세뇨관 간질 위축과 섬유화가 관찰되었고 석회화는 외부 수질 세뇨관 간질에서 관찰되었다.결 론: 저자들은 성인에서 furosemide 장기 복용이 신수질 석회화를 유발할 수 있으며 신수질 석회화 발생의 위험성은 furosemide 복용 용량과 관련이 있다는 것을 알 수 있었다. 저자들은 성인에서 우연히 신장 초음파나 컴퓨터 단층 촬영상 신수질 석회화 소견이 관찰되면 furosemide 장기 오용 여부를 반드시 감별진단 해야 한다고 제안한다. Background : The use of furosemide is well recognized as a predisposing factor to nephrocalcinosis (NC) in infants. Although furosemide is widely used for various clinical settings in adults, the association of furosemide use and nephrocalcinosis in adults is not well established. Methods : We studied 18 consecutive adult patients( male : female=1 : 17, age range 21-59 years) who took furosemide habitually to control their weights or edema for a long-term period(range 3-25 years). NC was evaluated using renal ultrasonography(US), computed tomography(CT) and/or kidney biopsies. Patients were categorized into NC(+) and NC(-) groups while the difference in clinical features were investigated. Results : Renal US and CT revealed nephrocalcinosis in the bilateral medullary pyramids in 15(83.3 %) out of 18 patients. The duration of furosemide abuse was not different between NC(+) and NC(-) groups(10.1±1.7 years vs. 15.3±0.9, p>0.05). The daily dose of furosemide was higher in NC(+) group than the NC(-) group(538±174 vs. 67±13 mg/day, p<0.01), however. All patients showed a variable degree of renal insufficiency and there was no difference in creatinine clearance between two groups(p>0.05). The kidney biopsies performed in three patients showed focal tubulointerstitial fibrosis and atrophy and calcifications were observed at outer medullary tubulointerstitium. Conclusion : Long-term furosemide abuse could cause medullary nephrocalcinosis in adults and the risk of developing of nephrocalcinosis is correlated with the daily dose of furosemide. We suggest that long-term furosemide abuse should be suspected in adult patients when medullary nephrocalcinosis is incidentally detected by US and/or CT.

시스틴증에서 각막의 시스틴 결정 축적

최윤주 ( Choe Yun Ju ) , 유정란 ( Yu Jeong Lan ) , 박미라 ( Park Mi La ) , 정성근 ( Jeong Seong Geun ) 대한안과학회 2003 대한안과학회지 Vol.44 No.7