제주해협의 해류와 월별 유량변화

노홍길,방익찬,김상현,현경훈,김준택,양영진,홍창수 제주대학교 해양연구소 1997 해양자원연구소연구보고 Vol.21 No.-

Currents are measured in the Straits of Cheju by detecting surface buoy tracks and mooring current meters in 1996-1997. As a result, north-eastward currents are decteted in the Straits of Cheju all the year round, which is weak in spring and strong in summer and fall. Average speeds of 20 cm/s to the east. 7 cm/s to the north and 22 cm/s to the north-east appeared in the surface. Currents are fast in the middle of the strait and slow near Cheju Island. East-west components of the currents are about 3 times faster than the north-south ones. Also. it is shown that surface buoys released within the distance of 6 miles away from Cheju do not drift out of the Straits of Cheju because of tongue-like warm waters appeared in the eastern entrance of the strait. Volume transports calculated by geostrophic calculation are shown to be 0.05-0.2 Sv in winter and 0.4-0.5 Sv in summer.

인천지역 대학생에 의한 대학급식소의 급식서비스에 대한 품질 평가

우경자,한복진,노정옥 동아시아식생활학회 2004 동아시아식생활학회지 Vol.14 No.3

This study was conducted to investigate the quality assessment of performance of the university foodservice. Self administered questionnaires were collected from 305 students living in Incheon. Statistical data analysis was completed using a SPSS v. 10.0 program. The results were summarized as follows: 61.4% of male students and 48.1% of female students responded to have lunch regularly. Only 23.4% of male students and 14.1% of female students used the university foodservice daily. Reasons for the irregularity of lunch were responded as "lecture", "eating when I want" and "appointment with friends", etc. The quantity, temperature, nutritional value, appearance, hygiene, taste and freshness of foods and price of menus were evaluated as appropriate but using seasonal foods, number of side-dishes, etc. as unsatisfactory. Service speed, cloth hygiene, neatness and kindness of employee were evaluated as appropriate. For the facilities of foodservice, counter location, menu board and lighting facilities were evaluated as appropriate but heating facilities, disponsition of tables and chairs of dining hall were as unsatisfactory. Sanitation of floors and walls of dining hall, restroom and utensils, etc. was evaluated as low.

복어중독에 의한 가사 상태에서 소생한 1예

송승찬,신진호,강석우,박경남,최호순,박근태,문희식,기춘석,이성희,윤병철,노우균,조균석,이민호 大韓應急醫學會 1998 대한응급의학회지 Vol.9 No.3

Tetrodotoxin is a neurotoxin produced by about 90 species of puffer fish and causes paralysis of central nervous system and peripheral nerves by blocking the movement of all monovalent cation. Ingestion of tetrodotoxin produces clinical manifestations such as paresthesias(within 10-45 min), vomiting, lightheadedness, salivation, muscle twitching, dysphagia, difficulty in speaking, convulsion and death that expressed by cardiopulmonary arrest with loss of brain stem reflex sometimes. Tetrodotoxin prevents or delays ischemia induced neuronal death by way of following 3 mechanisms. Firstly, it reduces the energy demand of the brain tissues. Secondly, it delays or even prevents anoxic depolarization. Finally, it deminishes ischemia induced cell swelling and cerebral edema. We report a case of puffer fish poisoning which presented with cardiopulmonary arrest and loss of brain stem reflex, but completely recovered by aggressive cardiopulmonary resuscitation.

정신분열병에 대한 리스페리돈의 효과 및 안정성

이민수,김용구,김영훈,연병길,오병훈,윤도준,윤진상,이철,정희연,강병조,김광수,김동언,김명정,김상훈,김희철,나철,노승호,민경준,박기창,박두병,백기청,백인호,손봉기,손진욱,양병환,양창국,우행원,이정호,이종범,이홍식,임기영,전태연,정영조,정영철,정인과,정인원,지익성,채정호,한상익,한선호,한진희,서광윤 大韓神經精神醫學會 1998 신경정신의학 Vol.37 No.1

연구목적 : 본 시험의 목적은 임상시험 시작전에 연구자들을 대상으로 PANSS Workshop을 통하여 PANSS, ESRS에 대한 국내에서의 표준화 작업을 구축하고 새로운 정신병 치료제인 리스페리돈의 효과와 안정성을 재확인하여 리스페리돈 사용에 대한 적정화를 이루는데 있다. 연구방법 : 1996년 4월부터 1996년 9월까지 국내 39개 대학병원 정신과에 입원중인 혹은 증상이 악화되어 입원하는 정신분열병 환자 377명을 대상으로 다시설 개방 연구를 시행하였다. 1주일간의 약물 배설기간을 가진후, 리스페리돈을 8주간 투여하였고, 기준점, 1주, 2주, 4주, 그리고 8주후에 평가되었다. 용량은 제1일에는 리스페리돈 1mg씩 1일 2회, 제2일에는 2mg씩 1일 2회, 제3∼7일에는 3mg씩 1일 2회 투여하였다. 이후 환자의 임상상태에 따라 임의로 증량할 수 있으며, 최대 일일 16mg을 초과하지 않도록 하였다. 추체외로 증상을 조절하기 위한 투약을 허용하였다. 임상증상 및 부작용의 평가는 PANSS(Positive and Negative Syndrome Scale), CGI(Clinical Global Impression) 그리고 ESRS(Extrapyramidal Symptom Rating Scale)을 사용하였다. 연구결과 : 377명중 343명(91%)이 8주간의 연구를 완결하였다. 치료 종결시점인 8주후 PANSS 총점수가 20% 이상 호전된 경우를 약물 반응군으로 정의할때, 약물반응군은 81.3%였다. 리스페리돈에 반응하는 예측인자로는 발병연령, 이전의 입원 횟수, 유병기간이 관련 있었다. 리스페리돈은 1주후부터 PANSS양성, 음성, 및 일반정신병리 점수상에 유의한 호전을 보여 효과가 빨랐다. CGI의 경우도 기준점에 비해 1주후부터 유의한 감소를 나타내었다. ESRS의 경우, 파킨슨 평가점수는 기준점과 비교해 투여 1주, 2주, 4주후 유의하게 증가되었다가 8주후 기준점과 차이가 없었다. Dystonia 평가점수는 1주후만 유의한 증가를 보였으며, dyskinesia 평가점수는 유의한 차이가 없었다. 혈압, 맥박수의 생명징후 및 일반 혈액학 검사, 생화학적 검사, 심전도 검사에서 유의한 변화는 없었다. 결 론 : 이상의 다시설 개방 임상 연구를 통해 리스페리돈은 정신분열병 환자에서 양성증상뿐만 아니라 음성증상 및 전반적인 증상에도 효과적인 것으로 사료된다. 보다 명확한 평가를 위해서는 다른 항정신병약물과의 이중맹검 연구가 필요할 것으로 생각되며, 또한 장기적 치료에 대한 평가도 함께 이루어져야 하겠다. Objective : The purpose of this study was to investigate the efficacy and safety of risperidone in the treatment of Korean schizophrenic patients. Method : This multicenter open study included 377 schizophrenic patients drawn from 39 university hospitals. After a wash-out period of 1 week, the schizophrenic patients were treated with risperidone for 8 weeks and evaluated at 5 points ; at baseline, and 1, 2, 4 and 8 weeks of treatment. The dose was increased from 2mg/day(1mg twice daily) to 6mg/day(3mg twice daily) during the first week and adjusted to a maximum of 16mg/day over the next 7 weeks according to the patient's clinical response. Medication to control extrapyramidal symptoms was permitted. The psychiatric and neurological status of the patients was assessed by PANSS, CGI, and ESRS scales. Results : 343(91%) of 377 patients completed the 8-week trial period. Clinical improvement, as defined by a 20% or more reduction in total PANSS score at end point, was shown by 81.3% of patients. The predictors of response to risperidone were associated older age, shorter duration of illness, fewer previous hospitalization. Risperidone had rapid onset of action ; a significant decrease of the total PANSS and three PANSS factor(positive, negative, general), and CGI was already noticed at the end of first week. For the ESRS, parkinsonism rating scores were significantly increased until week 4 comparing with baseline. Dystonia rating scores were significantly increased until week 1, and dyskinesia rating scores were not significantly changed during the study. Laboratory parameters including vital sign, EKG, hematological, and biochemical values showed no significant changes during the trial. Conclusions : This study suggests that risperidone is generally safe and effective against both the positive and negative symptoms in our group of patients.

Superior Efficacy and Selectivity of Novel Small-Molecule Kinase Inhibitors of T790M-Mutant EGFR in Preclinical Models of Lung Cancer

Rho, Jin Kyung,Lee, In Yong,Choi, Yun Jung,Choi, Chang-Min,Hur, Jae-Young,Koh, Jong Sung,Lee, Jaekyoo,Suh, Byung-Chul,Song, Ho-Juhn,Salgaonkar, Paresh,Lee, Jungmi,Lee, Jaesang,Jung, Dong Sik,Kim, Sang American Association for Cancer Research 2017 Cancer Research Vol.77 No.5

Animal models and therapeutic molecular targets of lung cancer

Jin Kyung Rho 한국실험동물학회 2019 한국실험동물학회 학술발표대회 논문집 Vol.2019 No.1

The application of transgenic mice with mutant EGFR in drug development and biological role

Jin Kyung Rho(노진경) 한국실험동물학회 2022 한국실험동물학회 학술발표대회 논문집 Vol.2022 No.1

p53 Enhances Gefitinib-Induced Growth Inhibition and Apoptosis by Regulation of Fas in Non-Small Cell Lung Cancer

Rho, Jin Kyung,Choi, Yun Jung,Ryoo, Baek-Yeol,Na, Im II,Yang, Sung Hyun,Kim, Cheol Hyeon,Lee, Jae Cheol American Association for Cancer Research 2007 Cancer research Vol.67 No.3

<P>Treatment with gefitinib, a specific inhibitor of epidermal growth factor receptor tyrosine kinase (EGFR-TK), has resulted in dramatic responses in some patients with non-small cell lung cancer (NSCLC). Most patients who respond to gefitinib have EGFR-TK mutations; however, >10% of patients with EGFR-TK mutations do not respond. Similarly, some patients without EGFR-TK mutations respond to this drug, suggesting that other factors determine sensitivity to gefitinib. Aberrations of the tumor suppressor gene p53 are frequently associated with drug resistance. In this study, we investigated the role of p53 in growth-inhibitory and apoptotic effects of gefitinib in the human NSCLC cell lines NCI-H1299 and A549, which have no EGFR-TK mutations. NCI-H1299 cells, which had a p53-null genotype, were more resistant to gefitinib compared with A549 cells, which were wild-type p53 (IC(50), 40 micromol/L in NCI-H1299 and 5 micromol/L in A549). Treatment of A549 with gefitinib resulted in the translocation of p53 from cytosol to nucleus and the up-regulation of Fas, which was localized to the plasma membrane. In the stable H1299 cell line with tetracycline-inducible p53 expression, induced p53 enhanced growth inhibition and apoptosis by gefitinib through the up-regulation of Fas and restoration of caspase activation. A caspase inhibitor, Z-VAD-fmk, reduced these effects. Conversely, inhibition of p53 using antisense oligonucleotide in A549 caused a significant decrease in apoptosis by gefitinib and down-regulation of Fas under the same conditions. In conclusion, p53 may play a role in determining gefitinib sensitivity by regulating Fas expression in NSCLC.</P>

Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1alpha.

Rho, Jin Kyung,Choi, Yun Jung,Lee, Jin Kyung,Ryoo, Baek-Yeol,Na, Im Ii,Yang, Sung Hyun,Kim, Cheol Hyeon,Yoo, Young Do,Lee, Jae Cheol National Hellenic Research Foundation 2009 ONCOLOGY REPORTS Vol.21 No.3

<P>Hypoxia-inducible factor-1alpha (HIF-1alpha) is a transcriptional factor which is activated by hypoxia and associated with cell survival, proliferation and drug resistance. Recent studies have shown that the down-stream molecules of the epidermal growth factor receptor (EGFR) signal are involved in the hypoxia-dependent or -independent HIF-1alpha protein accumulation. Thus, we hypothesized that an EGFR-TK inhibitor, gefitinib, might circumvent the hypoxia-induced drug resistance via the regulation of HIF-1alpha expression. In our data, treatment of gefitinib suppressed induced HIF-1alpha by hypoxia. This action of gefitinib was caused by reduced protein stability without any change in the level of HIF-1alpha mRNA. The effect of gefitinib on down-regulation of HIF-1alpha was reversed by transfection of constitutively active form of Akt. The cellular response to gefitinib was similar in both normoxia and hypoxia condition. However, the response to conventional chemotherapeutic drugs decreased >50% under hypoxia condition and they did not change HIF-1alpha expression. In addition, the suppression of HIF-1alpha using siRNA overcame partially hypoxia-induced drug resistance. In conclusion, gefitinib was able to circumvent hypoxia-induced drug resistance suggesting that the effective suppression of HIF-1alpha by the inhibition of EGFR-Akt pathway may overcome the hypoxia-induced drug resistance.</P>

The role of MET activation in determining the sensitivity to epidermal growth factor receptor tyrosine kinase inhibitors.

Rho, Jin Kyung,Choi, Yun Jung,Lee, Jin Kyung,Ryoo, Baek-Yeol,Na, Im Il,Yang, Sung Hyun,Lee, Seung Sook,Kim, Cheol Hyeon,Yoo, Young Do,Lee, Jae Cheol American Association for Cancer Research 2009 Molecular Cancer Research Vol.7 No.10

<P>The development of resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKI) seems almost inevitable, even in patients with lung cancer that initially respond well to EGFR-TKIs. MET amplification was recently found to be a mechanism of escape from the anticancer effect of EGFR inhibitors. In the present study, we investigated the means whereby MET affects sensitivity to EGFR-TKIs in PC-9 cells. Gefitinib- or erlotinib-resistant sublines were established by exposing the parental PC-9 cell line to chronic, repeated treatments with these drugs. These resistant sublines showed more than 100-fold more resistance to gefitinib and erlotinib and acquired cross-resistance to other EGFR-TKIs. The T790M EGFR mutation was found by pyrosequencing, and this seemed to be the cause of drug resistance. Resistant cells also showed MET activation, although gene amplification was not detected. Furthermore, the induction of MET activity was not found to be associated with sensitivity to EGFR-TKIs. Interestingly, increased passage number without exposure to gefitinib or erlotinib caused MET activation, but this did not affect sensitivity to EGFR-TKIs. In addition, hepatocyte growth factor was found to block the ability of EGFR-TKIs to inhibit MET activation. However, sustained MET activation by hepatocyte growth factor did not modulate the cellular effects of gefitinib or erlotinib. Rather, activated MET enhanced migration and invasion abilities. Summarizing, MET activation may be acquired during cancer cell proliferation and enhances migratory and invasive abilities without affecting cellular sensitivity to EGFR-TKIs. Accordingly, the present study suggests that MET activation caused by factors other than MET gene amplification is not a suitable surrogate marker of resistance to EGFR-TKIs.</P>