천장관절 증후군 환자에서 관절강 내 증식치료의 효과

이재담 ( Jae Dam Lee ),이대욱 ( Dae Wook Lee ),정철원 ( Cheol Won Jeong ),이형곤 ( Hyung Gon Lee ),윤명하 ( Myung Ha Yoon ),김웅모 ( Woong Mo Kim ) 대한통증학회 2009 The Korean Journal of Pain Vol.22 No.3

임상연구 : Remifentanil과 Lidocaine이 Sevoflurane 마취유도 시 기관내삽관에 필요한 흡입시간에 미치는 영향

이재담 ( Jae Dam Lee ),정창영 ( Chang Young Jeong ),최정일 ( Jeong Il Choi ),이형곤 ( Hyung Gon Lee ),정성태 ( Sung Tae Chung ),김웅모 ( Woong Mo Kim ) 대한마취과학회 2008 Korean Journal of Anesthesiology Vol.55 No.5

Background: This study was conducted to investigate the optimal time interval for tracheal intubation and the effect of adjuvant drugs such as remifentanil and lidocaine during induction and tracheal intubation using sevoflurane inhalation without muscle relaxant. Methods: This study enrolled patients with the age of 20-60 years old and ASA 1 or 2. Patients were randomly assigned into one of 4 groups (S, SR, SRL, SL), in which they were given remifentanil (R) i.v. at a rate of 0.25 μg/kg/min, or lidocaine (L) i.v. bolus of 1.5 mg/kg during sevoflurane inhalation (S). Anesthesia was performed as inhalation induction 2 minutes after pre-filling with sevoflurane 8 vol%. The time interval between induction and tracheal intubation was determined using up-and-down method. When satisfied all of the categories of response to tracheal intubation, the case was assigned to `success`, otherwise `fail`. In each groups, effective time for successful intubation in 50% (ET50) and 95% (ET95) were calculated by probit analysis. Results: ET50 was 3.90 minutes (95% confidence interval 3.32-4.38) in group S, 3.18 minutes (2.92-3.48) in group SL, 2.83 minutes (2.47-3.07) in group SR, and 2.68 minutes (2.37-2.95) in group SRL. In group S, SL, SR, and SRL, ET95 was 4.52 minutes (4.17-7.95), 3.63 minutes (3.37-4.97), 3.30 minutes (3.06-4.64), and 3.12 minutes (2.89-4.42), respectively. Conclusions: The optimal time to intubate successfully using sevoflurane without muscle relaxant in 95% patients was 4.5 minutes. The optimal time is reduced to 3.1 minutes by coadministration of remifentanil and lidocaine. (Korean J Anesthesiol 2008;55:565~9)

Bone Matrix Gelatin이 일차배양 골아세포의 DNA생합성에 미치는 영향

김기용(Key-Yong Lee),이춘성(Choon-Sung Lee),오원혁(Won-Hyeok Oh),김성재(Jung-Jae Kim),이재담(Jae-Dam Lee),조성우(Sung-Woo Cho),김금이(Geum-Yi Kim) 대한정형외과학회 1992 대한정형외과학회지 Vol.27 No.2

골절 치유 과정의 혈청 내 Alkaline Phosphatase와 Osteocalcin의 변화

이호승(Ho Seung Lee),이춘성(Choon Sung Lee),장재석(Jae Suk Jang),이재담(Jae Dam Lee),엄성문(Sung-Moon Um) 대한정형외과학회 2002 대한정형외과학회지 Vol.37 No.3

Interleukin-1이 골아세포주 UMR-106-1의 증식에 미치는 영향

이범구(Beom Koo Lee),김병직(Byung Jik Kim),이재담(Jae Dam Lee),김건범(Geon Beom Kim) 대한정형외과학회 1999 대한정형외과학회지 Vol.34 No.1

사람 혈소판에서 분리한 Transforming Growth Factor - β가 초회 배양된 Mesangial 세포의 복제 및 Collagen 합성에 미치는 영향

조성우,박수길,김금이,이희봉,이재담 ( Sung Woo Cho,Su Kil Park,Geum Yi Kim,Hee Bong Lee,Jae Dam Lee ) 생화학분자생물학회 1992 BMB Reports Vol.25 No.3

The effect of TGF-β on cell replication and collagen synthesis in primarily cultured mesangial cells from rats was studied in vitro. The TGF-β was purified from human platelets by acidic ethanol extraction and gel filtration with FPLC. The effect of TGF-β on the DNA synthesis and the collagen synthesis in mesangial cells depended on both TGF-β concentration and cell density in monolayer culture. Concentrations of TGF-β ranging from 0.1∼15 ng/ml were evaluated for their effects upon DNA synthesis. In confluent cells, when compared to the growth rate in standard medium, TGF-β concentrations in the range 0.1∼15 ng/ml reduced a cell proliferation up to 35%, suggesting inhibition of cell division. The effect of TGF-β on collagen synthesis in mesangial cells was biphasic. In confluent cells, the addition of TGF-β induced a 2-fold increase in the production of collagen when compared with cells grown in standard medium. The maximal effect of TGF-β occurred at 0.5 ng/ml. At higher concentrations there was a decrease in the action of TGF-β with the effects on collagen production. In subconfluent cells, however, TGF-β showed no significant effects on the DNA synthesis and the collagen synthesis at all concentrations. These results support that TGF-β may play an important role as a multifunctional regulator in the pathogenesis of glomerulosclerosis. v

패혈증 증후군환자에서 성인성 호흡곤란 증후군 발생의 예측 지표서의 혈중 Tumor Necrosis Factor-$\alpha$와 Interleukin-$1{\beta}$에 관한 연구

고윤석,장윤혜,김우성,이재담,오순환,김원동,Koh, Youn-Suck,Jang, Yun-Hae,Kim, Woo-Sung,Lee, Jae-Dam,Oh, Soon-Hwan,Kim, Won-Dong 대한결핵및호흡기학회 1994 Tuberculosis and Respiratory Diseases Vol.41 No.5

연구배경: ARDS발생 기전에 있어 TNF-$\alpha$나 IL-$1{\beta}$의 역할은 이들이 폐혈관 내피세포에 작용하여 모세혈관의 투과성을 증가시키는 것으로 추정되나 ARDS환자 발생 예측 지표로서의 TNF-$\alpha$ 및 IL-$1{\beta}$의 임상적 유용성에 대한 지금까지의 연구결과는 부정적이다. 이는 기존연구들이 다양한 질환들을 대상으로 함으로써 ARDS 발생기전의 다양성이 ARDS환자 발생 예측지표로서의 TNF-$\alpha$의 유용성을 부정적으로 나타나게하였을 가능성을 배제할 수 없다. 이에 저자들은 ARDS 발생이 내독소와 cytokines등에 의한 작용인 것으로 알려지고 있는 패혈증 증후군 환자들을 대상으로 TNF-$\alpha$와 IL-$1{\beta}$의 ARDS 발생의 예측 표지자로서 임상적 효용성을 검토하고자 본 연구를 시행하였다. 방법: 패혈증 증후군환자들을 대상으로 ARDS발생군(이하 ARDS군, 16명)과 호흡부전 상태에서 ARDS로는 진행하지않은 급성호흡 부전군(Acute hypoxemic respiratory failure group, 이하 AHRF군, 20명)으로 분류하여 등록시, 24시간 및 72시간후에 채혈하여 ARDS군은 ARDS 발생시에, AHRF군은 동맥혈 산소분압에 대한 폐포 산소분압의 비가 가장 낮은 시점의 TNF-$\alpha$와 IL-$1{\beta}$의 농도를 비교하였다. 또한 ARDS 및 AHRF군에서 쇽 발생군과 비발생군으로 분류하고 쇽 발생시에 측정된 TNF-$\alpha$와 IL-$1{\beta}$를 비발생군의 TNF-$\alpha$ 및 IL-$1{\beta}$의 값과 비교하였다. 대조군은 건강 대조군으로서 1회만 채혈하였다. 결과: 1) 혈중 TNF-$\alpha$의 농도: 본 연구에 사용한 Predicta kit의 TNF-$\alpha$ 농도 측정의 민감도는 평균${\pm}2$표준편차의 하한값이 10pg/mL이며, 특이도는 100%로, ARDS군 16명중 8명이, AHRF군 20명중 12명이 10pg/mL 이상으로 측정되어 두 군사이에서 혈중 TNF-$\alpha$가 10pg/mL 이상 발현된 비율의 차이는 없었다. ARDS 및 AHRF군의 혈중 TNF-$\alpha$의 중앙값 농도는 각각 10.26pg/mL(<10-16.99pg/mL, 사분위수범위, interquartile range), 10.82pg/mL(<10-20.38pg/mL)로서 두 군 사이에는 유의한 차이가 없었으며 (Fig. 1), ARDS 발생 전후의 혈중 TNF-$\alpha$의 농도도 중앙값이 10pg/mL미만(<10-15.32)pg/mL 및 10pg/mL미만(<10-10.22)pg/mL로서 유의한 차이가 없었고 6명중 2명만이 ARDS 발생 전에 비하여 TNF-$\alpha$의 값이 증가되었다. ARDS 및 AHRF군에서 패혈성 쇽이 발생한 환자들(26명)의 TNF-$\alpha$의 농도는 12.53(<10-20.82)pg/mL로서 비발생군(10명) <10pg/mL에 비해 유의하게 높았으나(p<0.01)(Fig. 2), 전체 생존군(<10, <10-12.92pg/mL)과 사망군(11.80, <10-20.8pg/mL)사이에는 유의한 차이가 없었다(P=0.28). 2) 혈중 IL-$1{\beta}$의 농도: 본 연구에 사용한 Quantikine kit의 최저 측정치는 0.3ng/mL로서 건강 대조군 10명중 1명을 제외한 모두에서 IL-$1{\beta}$측정치가 0.3pg/mL이하였다. ARDS 및 AHRF군의 검체 중 0.3ng/mL 이하로 측정된 경우는 ARDS, AHRF군에서 각각 1예가 있었다 ARDS 및 AHRF군의 혈중 IL-$1{\beta}$의 농도는 각각 2.22(1.37-8.01)ng/mL, 2.13(0.83-5.29)ng/mL으로서 두 군사이에는 유의한 차이가 없었으며(Fig. 3), ARDS 발생전(2.53, 0.3-8.38ng/mL)과 발생후(5.35, 0.66-11.51ng/mL)에서도 차이가 없었다. 패혈성 쇽 발생군(2.51, 1.28-8.34ng/mL)과 비발생군(1.46, 0.15-2.13ng/mL)사이에서는 통계적인 유의한 차이는 없었으나 비발생군에서 낮은 경향을 보였다(각각 P=0.44, P=0.054)(Fig. 4). 생존군과 Background: Tumor necrosis factor(TNF)-$\alpha$ and Interleukin(lL)-$1{\beta}$ are thought to play a major role in the pathogenesis of the septic syndrome, which is frequently associated with adult respiratory distress syndrome(ARDS). In spite of many reports for the role of TNF-$\alpha$ in the pathogenesis of ARDS, including human studies, it has been reported that TNF-$\alpha$ is not sensitive and specific marker for impending ARDS. But there is a possibility that the results were affected by the diversity of pathogenetic mechanisms leading to the ARDS because of various underlying disorders of the study group in the previous reports. The purpose of the present study was to evaluate the roles of TNF-$\alpha$ and IL-$1{\beta}$ as a predictable marker for development of ARDS in the patients with septic syndrome, in which the pathogenesis is believed to be mainly cytokine-mediated. Methods: Thirty-six patients of the septic syndrome hospitalized in the intensive care units of the Asan Medical Center were studied. Sixteens suffered from ARDS, whereas the remaining 20 were at the risk of developing ARDS(acute hypoxemic respiratory failure, AHRF). In all patients venous blood samples were collected in heparin-coated tubes at the time of enrollment, at 24 and 72 h thereafter. TNF-$\alpha$ and IL-$1{\beta}$ was measured by an enzyme-linked immunosorbent assay (ELISA). All data are expressed as median with interquartile range. Results: 1) Plama TNF-$\alpha$ levels: Plasma TNF-$\beta$ levels were less than 10pg/mL, which is lowest detection value of the kit used in this study within the range of the $mean{\pm}2SD$, in all of the normal controls, 8 of 16 subjects of ARDS and in 8 in 20 subjects of AHRF. Plasma TNF-$\alpha$ levels from patients with ARDS were 10.26pg/mL(median; <10-16.99pg/mL, interquartile range) and not different from those of patients at AHRF(10.82, <10-20.38pg/mL). There was also no significant difference between pre-ARDS(<10, <10-15.32pg/mL) and ARDS(<10, <10-10.22pg/mL). TNF-$\alpha$ levels were significantly greater in the patients with shock than the patients without shock(12.53pg/mL vs. <10pg/mL) (p<0.01). There was no statistical significance between survivors(<10, <10-12.92pg/mL) and nonsurvivors(11.80, <10-20.8pg/mL) (P=0.28) in the plasma TNF-$\alpha$ levels. 2) Plasma IL-$1{\beta}$ levels: Plasma IL-$1{\beta}$ levels were less than 0.3ng/mL, which is the lowest detection value of the kit used in this study, in one of each patients group. There was no significant difference in IL-$1{\beta}$ levels of the ARDS(2.22, 1.37-8.01ng/mL) and of the AHRF(2.13, 0.83-5.29ng/mL). There was also no significant difference between pre-ARDS(2.53, <0.3-8.34ngfmL) and ARDS(5.35, 0.66-11.51ng/mL), and between patients with septic shock and patients without shock (2.51, 1.28-8.34 vs 1.46, 0.15-2.13ng/mL). Plasma IL-$1{\beta}$ levels were significantly different between survivors(1.37, 0.4-2.36ng/mL) and nonsurvivors(2.84, 1.46-8.34ng/mL). Conclusion: Plasma TNF-$\alpha$ and IL-$1{\beta}$ level are not a predictable marker for development of ARDS. But TNF-$\alpha$ is a marker for shock in septic syndrome. These result could not exclude a possibility of pathophysiologic roles of TNF-$\alpha$ and IL-$1{\beta}$ in acute lung injury because these cytokine could be locally produced and exert its effects within the lungs.

체외순환후 혈중 Thromboxane $B_2$와 Endothelin-1 농도 변화에 미치는 Aprotinin의 효과

임청,윤태진,김연승,김승후,이재담,노준량,송명근,Lim, Cheong,Yun, Tae-jin,Kim, Yeon-seung,Kim, Seung-hoo,Lee, Jae-dam,Rho, Joon-Ryang,Song, Meong-Gun 대한흉부심장혈관외과학회 2000 Journal of Chest Surgery (J Chest Surg) Vol.33 No.3

Background: Thromboxane A2 and endothelin-1 are the potent vasoconstrictors affecting pulmonary pathophysiology in response to whole body inflammatin following CPB. Aprotinin, as an antiiflammatory agent, may decrease the release of such vasoactive substance from pulmonary tissues, preventing pulmonary hypertension after cardiopulmonary bypass. Material and Method: Ten mongrel dogs(Bwt. ac. 20kg) were subjected to cardioupulmonary bypass for 2 hours and postbypass pulmonary vascular resistance(0, 1, 2, 3 hours) were compared with prebypass level. The dogs were divided into 2 groups; control group(n-5) and aprotinin group(n=5). In the aprotinin group, aprotinin was administered as follows; 50,000 KIU/kg mixed in pump priming solution, 50,000 KIU/kg prebypass intravenous infusion over 30 minutes, 10,000 KIU/kg/hour postbypass continuous infusion. Prebypass and postbypass 0, 1, 2, 3 hour pulmonary vascular resistance were measured. At prebypass and postbypass 0, 90, 180 minutes, blood samples were obtained from pulmonary arterial and left atrial catherers for the assay of plasma thromboxane B2 a stable metabolite of thromboxane A2, and endothelin-1 concentrations. Result: The ratios of pustbypass over prebypass pulmonary vascular at postbypass 0, 1, 2, 3 hours were 1.28$\pm$0.20, 1.82$\pm$0.23, 1.90$\pm$0.19, 2.14$\pm$0.18 in control group, 1.58$\pm$0.18, 1.73$\pm$0.01, 1.66$\pm$0.10, 1.50$\pm$0.08 in aprotinin group ; the ratios gradually increased in control group while decreased or fluctuated after postbypass 1 hour in aprotinin group. There was statistically significant difference between control group and aprotinin group at postbypass 3 hours(P=0.014). Pulmonary arterial plasma concentration of thromboxane B2(pg/ml) at prebypass, postbypass 0, 90, 180 minutes were 346.4$\pm$61.9, 529.3$\pm$197.6, 578.3$\pm$255.8, 493.3$\pm$171.3 in control group, 323.8$\pm$118.0, 422.6$\pm$75.6, 412.3$\pm$59.9, 394.5$\pm$154.0 in aprotinin group. Left atrial concentrations were 339.3$\pm$89.2, 667.0$\pm$65.7, 731.2$\pm$192.7, 607.5$\pm$165.9 in control group, 330.0$\pm$111.2, 468.4$\pm$190.3, 425.4$\pm$193.6, 4.7.3$\pm$142.8 in aprotinin group. These results showed decrement of pulmonary thromboxane A2 generation in aprotinin group. Pulmonary arterial concentrations of endothelin-1(fmol/ml) at the same time sequence were 7.84$\pm$0.31, 13.2$\pm$0.51, 15.0$\pm$1.22, 16.3$\pm$1.73 in control group, 7.76$\pm$0.12, 15.3$\pm$0.71, 22.6$\pm$6.62, 14.9$\pm$1.11 in aprotinin group. Left atrial concentrations were 7.61$\pm$17.2, 57.1$\pm$28.4, 18.9$\pm$18.2, 31.5$\pm$20.5 in control group, 5.61$\pm$7.61, 37.0$\pm$26.2, 28.6$\pm$21.7, 37.8$\pm$30.6 in aprotinin group. These results showed that aprotinin had no effect on plasma endothelin-1 concentration after cardiopulmonary bypass. Conclusion: Administration of aprotinin during cardiopulmonary bypass could attenuate the increase in pulmonary vascular resistance after bypass. Inhibition of pulmonary thromboxane A2 generation was thought to be one of the mechanism of this effect. Aprotinin had no effect on postbypass endothelin-1 concentration.

Effects of Human Platelet Transforming Growth Factor-$\beta$ on Replication and Collagen Synthesis in Primarily Cultured Mesangial Cell

조성우,박수길,김금이,이희봉,이재담,Cho, Sung-Woo,Park, Su-Kil,Kim, Geum-Yi,Lee, Hee-Bong,Lee, Jae-Dam 생화학분자생물학회 1992 한국생화학회지 Vol.25 No.3

쥐의 mesangial 세포를 초회 배양하여 Transforming Growth Factor-$\beta$(TGF-$\beta$)가 세포의 복제 및 collagen 합성에 미치는 영향을 조사하였다. TGF-$\beta$는 사람 혈소판에서 산성 에탄올 침전법 및 FPLC를 이용한 젤 크로마토그래피의 방법으로 정제되었다. TGF-$\beta$가 mesangial 세포를 복제 및 collagen 합성에 미치는 영향은 TGF-$\beta$ 농도와 세포의 밀도에 따라 달라졌다. Confluent 세포의 경우 0.1~15 ng/ml의 농도에서 TGF-$\beta$는 mesangial 세포의 복제를 35%까지 감소시켰다. Collagen 합성은 0.5 ng/ml의 TGF-$\beta$ 농도에서는 2배로 증가되었으나 그 이상의 농도에서는 감소하기 시작하는 두 가지의 조절 양상을 보였다. 그러나 subconfluent 세포의 경우에는 세포의 복제 빛 collagen 합성 모두에 TGF-$\beta$는 아무런 효과를 나타내지 못하였다. 본 연구결과는 TGF-$\beta$가 glomerulosclerosis에 있어서 중요한 역할을 하리라는 가능성을 제시해주고 있다. The effect of TGF-$\beta$ on cell replication and collagen synthesis in primarily cultured mesangial cells from rats was studied in vitro. The TGF-$\beta$ was purified from human platelets by acidic ethanol extraction and gel filtration with FPLC. The effect of TGF-$\beta$ on the DNA synthesis and the collagen synthesis in mesangial cells depended on both TGF-$\beta$ concentration and cell density in monolayer culture. Concentrations of TGF-$\beta$ ranging from 0.1~15 ng/ml were evaluated for their effects upon DNA synthesis. In confluent cells, when compared to the growth rate in standard medium, TGF-$\beta$ concentrations in the range 0.1~15 ng/ml reduced a cell proliferation up to 35%, suggesting inhibition of cell division. The effect of TGF-$\beta$ on collagen synthesis in mesangial cells was biphasic. In confluent cells, the addition of TGF-$\beta$ induced a 2-fold increase in the production of collagen when compared with cells grown in standard medium. The maximal effect of TGF-$\beta$ occurred at 0.5 ng/ml. At higher concentrations there was a decrease in the action of TGF-$\beta$ with the effects on collagen production. In subconfluent cells, however, TGF-$\beta$ showed no significant effects on the DNA synthesis and the collagen synthesis at all concentrations. These results support that TGF-$\beta$ may play an important role as a multifunctional regulator in the pathogenesis of glomerulosclerosis.

혈소판이 소 폐동맥 내피세포의 Endothelin 생산에 미치는 효과

이상도 ( Sang Do Lee ),심태선 ( Tae Sun Shim ),권석운 ( Seog Woon Kwon ),류진숙 ( Jin Sook Ryu ),이재담 ( Jae Dam Lee ),임채만 ( Chae Man Lim ),고윤석 ( Youn Suck Koh ),김우성 ( Woo Sung Kim ),김동순 ( Dong Soon Kim ),김원동 ( Won 대한결핵 및 호흡기학회 1997 Tuberculosis and Respiratory Diseases Vol.44 No.5