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성태호,이정윤,김유일,김효석,권태근,김태호,김창환,장재혁 대한췌장담도학회 2023 대한췌담도학회지 Vol.28 No.4
호산구성 장염에 의한 급성 췌장염은 매우 드문 질환으로 증상 및 검사실 소견이 특별하지 않아 진단이 어렵다. 급성 췌장염의 원인이 명확하지 않은 경우, 가능한 원인으로 매우 드물지만 호산구성 위장염이 있을 수 있으며, 본 저자들은 호산구성 위십이지장염에 의해 발생한 재발성 급성 췌장염을 진단하고 류코트리엔 수용체 길항제로 치료하였던 증례를 문헌고찰과 함께 보고한다. Acute pancreatitis caused by eosinophilic gastroenteritis is a rare disease, and little has been reported so far. Diagnosing eosinophilic gastroenteritis is difficult because the symptoms and laboratory findings are not specific. We report a rare case of eosinophilic gastroenteritis related to acute pancreatitis as a possible cause of idiopathic acute pancreatitis. A 61-year-old man visited the hospital complaining of epigastric pain. Although no pancreatic abnormalities were confirmed on imaging studies, the patient showed hyperamylasemia and hyperlipasemia. Serum eosinophil fractions were initially normal. However, they were elevated on follow-up examinations, and a large number of eosinophils were observed in the biopsies of the stomach and duodenum, which led to the diagnosis of eosinophilic gastroduodenitis related to acute pancreatitis.
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중금속에 의한 HL-60 세포의 Apoptosis 유도
김남송,성태호,조광호,염정호,고대하 大韓産業醫學會 1999 대한직업환경의학회지 Vol.11 No.4
Objectives : Apotosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metal are well described, little is known about the mechanism of apoptosis by heavy metal toxicity. This study is designed to define the induction of apoptosis by which heavy metals exert the cytotoxic effect on human promyelocytic leukemic HL-60 cells. Methods : After the incubation with CdCl2, Na2SeO3 and HgC12, viability of the cells were measured by MTT assay. DNA fragmentation was analyzed by electrophoresis. For measurement of caspase 1 and 3-like proteases activity, the whole lysates were subjected to the proteolytic cleavage and then measured by using fluorospectrometry. c-JUN N-terminal kinase (JNK) activity was detected by an in vitro kinase assay. Transcriptional activities of activating protein-1 (AP-1) and nuclear factor-kB (NF-kB) were measured by electrophoresis mobility shift assay (EMSA). Results : Cadmium (120μM) and selenium (30μM) induce the apoptosis of HL-60 cells which is characterized by the ladder pattern of DNA fragmentation. Cadmium and selenium induce the activation of caspase-3 in a time dependent manner. They also increase the phosphotransferase activities of c-JUN N-terminal kinase (JNK) in cadmium and selenium treated HL-60 cells. Furthermore, cadmium and selenium increase the activation of transcriptional factors including AP-1 and NF-kB. Conclusions : These results suggest that cadmium and selenium induce the apoptotic death of HL-60 cells via activation of DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-kB.
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황찬웅,박한기,이용선,성태호,최재혁 한국과학기술원 반도체설계교육센터 2023 IDEC Journal of Integrated Circuits and Systems Vol.9 No.4
This work presents a low-jitter ring-oscillator-based digital PLL (RO-DPLL). To achieve low jitter, the proposed RO-DPLL used calibration techniques to optimize the gain of the Proportional-path (P-path) and Integral-path (I-path) in the digital-loop-filter (DLF) simultaneously. Since the effect of flicker noise increases as the frequency increases, the frequency drift of the RO-DPLL becomes more severe in the operation of the RO-DPLL. Thus, it is critical to calibrate the gain of the I-path to an optimal value because I-path of DLF compensates for the frequency error of the PLL. Moreover, the optimally-spaced time-to-digital-converter (OS-TDC) with the threshold calibrator provides sufficient information, supporting the efficient operation of the calibrators. Due to the use of the P/I-path co-optimization (PICO) and OS-TDC with calibrator, the proposed RO-DPLL achieved the rms jitter of 343 fs and the reference spur of –65dBc. And, its FoMjitter,N was –258.5 dBc, comparable to the state-of-the-art RO-based analog PLLs.
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세포 내 신호전달과정을 통한 카드뮴의 Apoptosis 유도
김남송,오경재,조광호,현미선,김유창,성태호,염정호,권근상 大韓産業醫學會 2002 대한직업환경의학회지 Vol.14 No.1
Objectives : Apoptosis is a process of active cell death, distinct from necrosis and characterized by specific morphological and biochemical features. Apoptosis induced by metals and metal-related deleterious conditions has only recently been studied. Although the toxic effects of heavy metals are well described, little is known about the mechanism of apoptosis via cadmium toxicity. Thereforce, this study is designed to define the induction mechanism of apoptosis by which cadmium exerts its cytotoxic effect on human promyelocytic leukemic HL-60 cells. The cytotoxic effects of cadmium on HL-60 cells are studied in regards to apoptotic signal transduction pathways. Methods : The mode of cadmuim-induced apoptosis was investigated in HL-60 cells. HL-60 cells were treated with various concentrations of cadmium and antioxidants after which the viability of the cells were measured by MTT assay. The morphological features of cadmium- induced apoptosis were evaluated by fluoromicroscopy and the DNA fragmentation was analyzed using 1.5% agarose gel electrophorosis. Kinase activity was assayed by autoradiography and activity of NF-κB and nuclear proteins were measured by EMSA. Results : Cadmium (125 μM) induces the characteristic morphological features of apoptosis, which are characterized by a shrinkage of the cytoplasm and a condensation of chromatin. In addition, cadmium induced the ladder pattern of DNA fragmentation. Antioxidants(Sodium nitroprusside, glutathione and N-acethylcysteine), which were not toxic to the cells, did not suppress apoptosis induced by cadmium. Cadmium enhances the expression of several classes of genes at elevated cytotoxic concentrations. Poly(ADP-ribose) polymerase(PARP) was predominantly in the fragmented form when doses of 125 μM were used. Since PARP is cleaved by CPP32 (caspase-3), we next determined if cadmium was capable of effecting changes in CPP32 activity. The results of these experiments showed that cadmium increased caspase-3 activity in a time dependent manner, corresponding to the time of appearance of fragmented PARP. Cadmium also increased the phosphotransferase activities of c-JUN N-terminal kinase(JNK). Furthermore, cadmium increased the activation of transcriptional factors including the activation of protein-1 (AP-1) and NF-κB. Conclusions : These results suggest that cadmium induces the apoptotic death of HL-60 cells via the activation of a DEVD-specific caspase, JNK and transcriptional factors such as AP-1 and NF-κB.
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