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조재화 ( Jae Hwa Cho ),윤용한 ( Young Han Yoon ),곽승민 ( Seung Min Kwak ),이홍렬 ( Hong Lyeol Lee ),김광호 ( Kwang Ho Kim ),백용수 ( Yong Soo Baek ),류정선 ( Jeong Seon Ryu ),홍성빈 ( Seong Bin Hong ),유성수 ( Sung Soo Yoo ),유 대한결핵 및 호흡기학회 2006 Tuberculosis and Respiratory Diseases Vol.61 No.6
We report a case of pulmonary adenocarcinoma complicated by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) following adjuvant chemotherapy. A 51-year-old woman with stage ⅢA adenocarcinoma received left lower lobe lobectomy in July, 2006. And then combination chemotherapy with paclitaxel and cisplatin was given to the patient. In five days after completion of second cycle of the chemotherapy, she visited emergency room because of general weakness and seizure. Her brain MRI was shown to be no evidence of brain metastasis. Serum sodium, urine and plasma osmolarities were 117mEq/L, 589 and 244mOsm/kg, respectively. She was improved with fluid restriction. Although occurrence of SIADH following chemotherapy is rare, physician should give an attention the potential for development of SIADH in the course of chemotherapyin non-small cell lung cancer patient. (Tuberc Respir Dis 2006; 61: 591-594)
조재식(Jae Sik Cho),이은직(Eun Jig Lee),김경래(Kyung Rae Kim),이경미(Kyeong Mi Lee),남문석(Moon Suk Nam),조재화(Jae Hwa Cho),신은택(Eun Tack Shin),임승길(Sung Kil Lim),이현철(Hyun Chul Lee),허갑법(Kap Bum Huh),김정호(Jeong Ho Kim),송경 대한내과학회 1994 대한내과학회지 Vol.47 No.1
N/A Background: Thyroid hormone closely relates with lipid metabolism and especially Hypothyroidism associates with hypercholesterolemia which accelerates atherosclerosis. The purpose of this study was to determine the relationship between thyroid disease and Lp (a). Methods: We evaluated 14 patients with hypothyroidism, 24 patients with hyperthyroidism and 50 normal subjects. Serum Lp (a) was measured by ELISA (IM- MUNOZYM GMBH, Germany), thyroid hormones were measured by ELISA and other lipid profiles by conventional methods. Results: Serum Lp(a) concentrations (median) of hypothyroidism (29.3 mg/dl) were significantly higher than those of hyperthyroidism (4 mg/dl and controls (10 mg/dl)(p<0.05), Total cholesterol and LDL-cholesterol of hypothyroidism (199.0±75.7 mg/dl, 134.6±57.5 mg/dl) were patients had higher total cholesterol (136.1±31.2 mg/dl) and LDL-cholesterol (66.7±31.4 mg/dl) than controls (p<0.05). Serum Lp (a) concentration had negative correlation with the levels of serum T₃, T₄, FT₄ and positive correlation with TSH (p<0.05). Conclusion: These results suggest that thyroid hormones have an influence on Lp (a) concentration.
금속 코일 색전술로 치료된 기관지 확장증이 동반된 기관지 동맥류
정현정 ( Hyun Jung Chung ),조재화 ( Jae Hwa Cho ),박병도 ( Byoung Do Park ),류정선 ( Jeong Seon Ryu ),곽승민 ( Seung Min Kwak ),이홍렬 ( Hong Lyeol Lee ),전용선 ( Yong Sun Jeon ) 대한결핵 및 호흡기학회 2008 Tuberculosis and Respiratory Diseases Vol.65 No.6
Bronchial artery aneurysm (BAA) is a rare entity that requires early diagnosis and immediate treatment due to the possibility of a life-threatening massive hemorrhage through rupture. The standard treatment is a surgical resection of the aneurismal artery. However, various embolization techniques, including coil embolization, are currently used as the optimal treatment because they are less invasive. A 65-year-old woman was referred for the treatment of intermittent hemoptysis. A chest CT scan showed an approximately 2 cm sized vascular mass with strong contrast enhancement originating from the right bronchial artery on the bronchiectatic parenchyma. On the angiogram, the inferior portion of the bronchial artery with a hypertrophic aspect and a huge bronchial artery aneurysm was detected on the left side branch. The bronchial artery aneurysm was embolized successfully with coils at the proximal and distal portion of the aneurysm. After coil embolization, the selective bronchial angiogram confirmed complete occlusion. We report this case of a bronchial artery aneurysm that was treated successfully with coil embolization. (Tuberc Respir Dis 2008;65:546-549)
조철호,곽승민,문태훈,조재화,류정선,이홍렬,Cho, Chul-Ho,Kwak, Seung-Min,Moon, Tae-Hun,Cho, Jae-Hwa,Ryu, Jeong-Seon,Lee, Hyong-Lyeol 대한결핵및호흡기학회 1999 Tuberculosis and Respiratory Diseases Vol.47 No.5
연구배경: 세포성장은 세포증식과 세포죽음의 균형에 의해 이루어 진다. 세포성장에 관여하는 여러 growth factor증 IGF-I은 IGF-IR와 결합하여 세포증식을 유발하는 mitogen으로 알려져 있다. 또한 IGF-I에 결합하는 IGFBPs중에 IGFBP-3는 혈액내에 가장 많은 carrier protein으로, IGF-I과 결합하여 IGF-I의 세포증식 효과를 증가 혹은 억제시킨다. 방 법: 3T3 fibroblast 세포를 이용하여 IGF-I과 IGF-IR transcripts를 northern blot으로 확인하고, IGF-I에 의한 mitogenic effect를 MTT assay 및 $^3H$-thymidine incorporation test로 관찰하고, IGF-I의 receptor인 IGF-IR의 활성화를 보기 위해 intracellular $\beta$-subunit의 tyrosine kinase domain의 phosphorylation을 western blot으로 관찰하였다. 또한 IGFBP-3가 3T3 세포에서 mitogenic effect에 미치는 영향을 보기 위해 anti-IGFBP-3와 ${\alpha}IR_3$을 단독 및 병용투여하여 관찰하였다. 결 과: 3T3 세포는 IGF-I와 IGF-IR의 mRNA expression을 보였으며, IGF-I을 투여시 IGF-IR의 intracelluar cytoplasmic protein인 $\beta$-subunit의 tyrosine kinase domain을 phosphorylation시켜 활성화시키며, 5%, 1% serum-containing media에서 세포증식을 보였으나, serum-free media에서는 세포증식을 보이지 않았다. 또한 anti-IGFBP-3 투여와 ${\alpha}IR_3$과 anti-IGFBP-3를 병용투여시는 세포종식이 각각 2배이상 증가하였으나, ${\alpha}IR_3$을 4시간 전처치후 ${\alpha}IR_3$과 anti-IGFBP-3를 병용투여시는 anti-IGFBP-3에 의한 세포종식이 보이지 않은 것으로 보아 IGF -I/IGFBP-3 결합에서 분리되는 free IGF-I어l 의해 세포증식이 유도된 것으로 생각된다. 결 론: IGF-I은 IGF-IR를 phosphorylation시켜 mitogenic effect를 보이며, IGFBP-3는 IGF-I의 mitogenic effect를 억제하는 것으로 생각된다. Background: Cell growth is a balance between cell proliferation and cell death. Insulin-like growth factor-I(IGF-I), which binds IGF-I receptor(IGF-IR), mediates cellular proliferation as a potent mitogen. IGF binding protein-3(IGFBP-3) as a circulating major IGFBP can inhibit or enhance the effects of IGF-I on cellular growth by binding IGFs. Methods: We investigated the expressions of mRNA of IGF-I and IGF-IR by northern blot and phosphorylation of IGF-IR with the treatment of IGF-I by western blot in 3T3 fibroblast cells. The cellular proliferations of 3T3 cells with the treatments of IGF-I were evaluated using $^3H$-thymidine incorporation and MTT assay. Also to observe the effect of IGFBP-3 on cellular proliferation, 3T3 cells were treated with anti-IGFBP-3 and ${\alpha}IR_3$(monoclonal antibody to IGF-IR) alone or in combination. Results: Our results demonstrated that 3T3 cells showed mRNA expressions of IGF-I and IGF-IR and the IGF-I increased phosphorylation of IGF-IR. The treatments of 3T3 cells with IGF-I increased cellular proliferation in 5 % and 1 % seruma-containing media, not in serum-free media. The addition of anti-IGFBP-3 to neutralize IGFBP-3 showed 2-fold increase of cellular proliferation, and also co-incubation of anti-IGFBP-3 and ${\alpha}IR_3$ together showed similar increase of cellular proliferation in 3T3 cells. Interestingly, when the cells were pretreated with ${\alpha}IR_3$ for 4 hr, prior to the simultaneous addition of ${\alpha}IR_3$ and anti-IGFBP-3, anti-IGFBP-3-mediated cellular proliferation was decreased to control level. All of these results suggest that free IGF-I released from IGF-I/IGFBP-3 complex would be involved in the cellular proliferation. Conclusion: IGF-I is a mitogen through the activation of IGF-IR in 3T3 cells, and IGFBP-3 could be a potent inhibitor for IGF-I action by binding IGF-I.