분산시스템에서 데드락 예방을 위한 데이터 우선순위 상속 알고리즘

노치환(ChiHawan Loe),서창석(ChangSuk Seo),이병욱(ByungWook Lee) 한국멀티미디어학회 1998 한국멀티미디어학회 학술발표논문집 Vol.1998 No.2

C / S 환경의 매핑 시스템 개발을 위한 복제 일관성 모델의 설계 및 구현 ( Design and Implementation of Replication Consistency Model for Mapping System in C / S )

김태헌,노치환,이병욱 대한전자공학회 1997 대한전자공학회 학술대회 Vol.1997 No.11

전국 하천수 중 잔류우려 농약 실태조사

황인성,오예진,권혜영,노진호,김단비,문병철,오민석,노현호,박상원,최근형,류송희,김병석,오경석,임치환,이효섭 한국환경농학회 2019 한국환경농학회지 Vol.38 No.3

BACKGROUND: This study was carried out to investigate pesticide residues from fifty streams in Korea. Water samples were collected at two times. Thee first sampling was performed from april to may, which was the season for start of pesticide application and the second sampling event was from august to september, which was a period for spraying pesticides multiple times. METHODS AND RESULTS: The 136 pesticide residues were analyzed by LC-MS/MS and GC/ECD. As a result, eleven of the pesticide residues were detected at the first sampling. Twenty eight of the pesticide residues were detected at the second sampling. Seven pesticides were frequently detected from more than 10 water samples. Ecological risk assessment (ERA) was carried out by using residual and toxicological data. Four scenarios were applied for the ERA. Scenario 1 and 2 were performed using LC50 values and mean and maximum concentrations. Scenarios 3 and 4 were conducted by NOEC values and mean and maximum concentrations. CONCLUSION: Frequently detected pesticide residues tended to coincide with the period of preventing pathogen and pest at paddy rice. As a result of ERA, five pesticides (butachlor, carbendazim, carbofuran, chlorantranilprole, and oxadiazon) were assessed to be risks at scenario 4. However, only oxadiazon was assessed to be a risk at scenario 3 for the first sampling. Oxadiazon was not assessed to be a risk at the second sampling. It seems to be temporary phenomenon at the first sampling, because usage of herbicides such as oxadiazon increased from April to march for preventing weeds at paddy fields. However, this study suggested that five pesticides which were assessed to be risks need to be monitored continuously for the residues.

Immediate Breast Reconstruction Does Not Have a Clinically Significant Impact on Adjuvant Treatment Delay and Subsequent Survival Outcomes

백승호,배순준,윤창익,박소은,차치환,안성귀,김영석,노태석,정준 한국유방암학회 2019 Journal of breast cancer Vol.22 No.1

Purpose: The use of immediate breast reconstruction (IBR) has been debated because it may be a causative factor in adjuvant treatment delay and may subsequently increase the probability of recurrence. We investigated whether IBR was related to adjuvant treatment delay and survival outcomes. Methods: We retrospectively analyzed the duration from operation to adjuvant treatment administration and survival outcomes according to IBR status among patients with breast cancer who underwent mastectomy followed by adjuvant chemotherapy from January 2005 to December 2014. Propensity score matching was performed to balance the clinicopathologic baseline characteristics between patients who did and did not undergo IBR. Results: Of 646 patients, 107 (16.6%) underwent IBR, and the median follow-up was 72 months. The median duration from surgery to adjuvant chemotherapy was significantly longer in patients who underwent IBR than in those who did not (14 vs. 12 days, respectively, p = 0.008). Based on propensity score matching, patients who underwent IBR received adjuvant therapy 3 days later than those who did not (14 vs. 11 days, respectively, p = 0.044). The duration from surgery to post-mastectomy radiation therapy (PMRT) did not significantly differ between the 2 groups. Local recurrence-free survival, regional recurrence-free survival, systemic recurrence-free survival, and overall survival were also not significantly different between the 2 groups (p = 0.427, p = 0.445, p = 0.269, and p = 0.250, respectively). In the case-matched cohort, survival outcomes did not change. Conclusion: IBR was associated with a modest increase in the duration from surgery to chemotherapy that was statistically but not clinically significant. Moreover, IBR had no influence on PMRT delay or survival outcomes, suggesting that it is an acceptable option for patients with non-metastatic breast cancer undergoing mastectomy.

우연히 발견된 충수돌기 점액종류 1예

권성일,김규종,이지영,김동완,노치환,박무인,박선자,구자영,백승언 고신대학교 의학부 2000 高神大學校 醫學部 論文集 Vol.15 No.1

Mucocele of the appendix is an uncommon disorder which is rarely diagnosed prior to a laparotomy. With progress in diagnostic procedures, such as the use of colonoscopy, ultrasonography, and computed tomography, preoperative diagnosis of the appendiceal mucocele has become possible. There have been several reported cases of appendiceal mucocele in which various symptoms and signs were present. In this case, a 50-year old female patient visited our hospital because of constipation and rectal bleeding, and then she had an incidental finding of mucocele of the appendix during colonoscopic evaluation for constipation and rectal bleeding. We have experienced the case of preoperatively diagnosed appendiceal mucocele by a colonoscopy and abdominal CT and barium enema in which she was operated and the surgical specimen revealed appendiceal mucocele.

인체위암세포주 (AGC)의 증식에 미치는 lovastatin의 억제효과

김지연,김성훈,서수홍,최병주,김현영,노치환,김동완,김기환,박무인,구자영 고신대학교(의대) 고신대학교 의과대학 학술지 2002 고신대학교 의과대학 학술지 Vol.17 No.1

Background : At the first step of cholesterol synthesis, 3-hydroxy-3-methylglutaryl-CoA reductase (HMG-CoA reductase) catalyzes the formation of mevalonate, which is the precusor of isoprenoid moieties that are incorporated into or linked to several molecules for cell growth and replication, which include Ras, Rho, G proteins and nuclear laminin B. Lovastatin (mevinolin), as an inhibitor of HMG-CoA reductase, blocks mevalonate synthesis, by which also prevents the isoprenylation of several proteins such as Ras, display antitumor effect in experimental models. In the present study the isoprenylation of several proteins such as Ras, display antitumor effect in experimental models. In the present study the effects of lovastatin on the growth of human gastric carcinoma cell line, AGS cells were examined and the effects of 5-fluorouracil (5-FU) were also stuided. Cell cycle analysis was done to examine the mechanisms for the inhibitory effects of lovastatin. Methods : The growth of ACS cells were examined by counting cell number on one and three days treatment with 0.2 umol/L, 0.4 umol/L, 0.8 umol/L, 1.6 umol/L, 3.2 umol/L lovastatin, and 0.1 ug/ml, 0.3 ug/ml 5-FU, after plating AGS cells into 35n㎡ plastic dishes at a density of 10*10^4 cells/dish. The reversibility of the effects of lovastatin was examined on one day to seven days treatment with 0.8 umol/L lovastatin after seeding 10*10^4 cells/dish. To examine the mechanisms for the inhibitory effects of lovastatin, cell cycle analysis was done on the cells after four days treatment with 0.8 umol/L lovastatin. Results : Lovastatin significantly inhibited the growth of AGS cells in a dose-dependent fashion (p<0.05). Forty-eight percent inhibiton of growth was found at an lovastatin concentration of 0.8 umol/L and ninety-three percent inhibition of growth was found at an lovastatin concentration of 3.2 umol/L after 4 days treatment. The inhibitory effect of media change after 24 hours treatment of lovastatin was note different from that of control group, which was not treated by lovastatin. Lovastatin combined with 5-FU significantly inhibited the growth of AGS cells in a dose-dependent fashion compraed to lovastatin or 5-FU alone (p<0.05), which suggested additive effect of the two drugs. After four days treatment with 0.8 umol/L lovastatin, the fraction of cells in G0-G1 phase, S phase and G2-M phase was 51.5%, 31.5%, 17.0% respectively in the control group, and 50.6%, 32.6%, 16.7% in the lovastatin group (0.8 umol/L), showing no significant differences between the two. Conclusions : Lovastatin significantly inhibited the growth of AGS cells in a dose-dependent fashion. The inhibitory effect for lovastatin on the growth of AGS cells was reversible since the growth of AGS cells after removal of lovastatin by a media change after 24-48 hours treatment of lovastatin was note different from that of control group which was note treated by lovastatin. The reversibility of growth inhibition suggests that lovastatin is not a non-specific cytotoxin for AGS cells. This is the first report that lovastatin may be very useful for the treatment of gastric carcinoma, especially in conjunction with 5-FU, because the concentrations (0.2-3.2 umol/L) used in our study were within the ranges of steady-state concentrations (0.15-0.3 umol/L) attainable in human serum by chronic administration of maximum recommended dose (80 mg/day) of lovastatin and additive effect of lovastatin and 5-FU. More studies by animal experiments and clinical trials are needed to establish lovastatin as an anticancer drug for human gastric carcinoma.

인체위암세포주(AGC)의 증식에 미치는 lovastatin의 억제효과

김지연,김성훈,서수홍,최병주,김현영,노치환,김동완,김기환,박무인,구자영 고신대학교 의학부 2002 高神大學校 醫學部 論文集 Vol.17 No.1

Background At the first step of cholesterol synthesis, 3-hydroxy-3-methylglutaryl-CoA reductase(HMG-CoA reductase) catalyzes the formation of mevalonate, which is the precusor of isoprenoid moieties that are incorporated into or linked to several molecules for cell growth and replication, which include Ras, Rho, G proteins and nuclear laminin B. Lovastatin(mevinolin), as an inhibitor of HMG-CoA reductase, blocks mevalonate synthesis, by which also prevents the isoprenylation of several proteins such as Ras, display antitumor effect in experimental models. In the present study the effects of lovastatin on the growth of human gastric carcinoma cell line, AGS cells were examined and the effects of 5-fluorouracil(5-FU) were also studied. Cell cycle analysis was done to examine the mechanisms for the inhibitory effects of lovastatin. Methods The growth of AGS cells were examined by counting cell number on one and three days treatment with 0.2umol/L, 0.4umol/L, 0.8umol/L, 1.6umol/L, 3.2umol/L lovastatin, and 0.1umol/L, 0.3㎍/㎖ 5-FU, after plating AGS cells into 35㎚^(2) plastic dishes at a density of 10*10^(4) cells/dish. The reversibility of the effects of lovastatin was examined on one day to seven days treatment with 0.8u㏖/L lovastatin after seeding 10*10^(4) cells/dish. To examine the mechanisms for the inhibitory effects of lovastatin, cell cycle analysis was done on the cells after four days treatment with 0.8u㏖/L lovastatin. Results Lovastatin significantly inhibited the growth of AGS cells in a dose-dependent fashion(p<0.05). Forth-eight percent inhibition of growth was found at an lovastatin concentration of 0.8umol/L and ninety-three percent inhibition of growth was found at an lovastatin concentration of 3.2umol/L after 4 days treatment. The inhibitory effect of lovastatin on the growth of AGS cells was firstly shown at the concentration of 0.4umol/L. The removal of lovastatin by a media change after 24 hours treatment of lovastatin was note different from that of control group, which was not treated by lovastatin. Lovastatin combined with 5-FU significantly inhibited the growth of AGS cells in a dose-dependent fasion compared to lovastatin or 5-FU alone(p<0.05), which suggested additive effect of the two drugs. After four days treatment with 0.8umol/L lovastatin, the fraction of cells in G0-G1 phase, S phase and G2-M phase was 51.5%, 31.5%, 17.0% respectively in the control group, and 50.6%, 32.6%, 16.7% in the lovastatin group(0.8umol/L), showing no significant differences between the two. Conclusions Lovastatin significantly inhibited the growth of AGS cells in a dose-dependent fashion, The inhibitory effect for lovastatin on the growth of AGS cells was reversible since the growth of AGS cells after removal of lovastatin by a media change after 24-48hours treatment of lovastatin was note different from that of control group which was note treated by lovastatin. The reversibility of growth inhibition suggests that lovastatin is not a non-specific cytotoxin for AGS cells. This is the first report that lovastatin may be very useful for the treatment of gastric carcinoma, especially in conjunction with 5-FU, because the concentrations(0.2-3.2umol/L) used in our study were within the ranges of steady-state concentrations(0.15-0.3umol/L) attainable in human serum by chronic administration of maximum recommended dose(80/㎎/day) of lovastatin and additive effect of lovastatin and 5-FU. More studies by animal experiments and clinical trials are needed to establish lovastatin as an anticancer drug for human gastric carcinoma.