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Lee, Hyuk,Lee, Jong Kyun,Kang, Seok Seon,Choi, Dongil,Jang, Kee-Tack,Kim, Jeong Hwan,Lee, Kyu Taek,Paik, Seung Woon,Yoo, Byung Chul,Rhee, Jong Chul G. Thieme 2007 Hepato-gastroenterology Vol.54 No.79
<P>BACKGROUND/AIMS: The differential diagnosis of early-stage pancreatic cancer and mass-forming pancreatitis is still unsettled. The purpose of the present study was to define the differential feature of focal mass-forming pancreatitis and malignant mass using aspects of clinical, laboratory and imaging features on pancreatogram or computed tomography (CT). METHODOLOGY: Between April 1995 and May 2003, 15 patients confirmed as inflammatory mass after surgical resection for pancreatic mass and 21 patients with early-stage pancreatic adenocarcinoma among the patients diagnosed as pancreatic malignancy were included in our study. Hospital records, laboratory results, findings of imaging studies and pathological findings were reviewed retrospectively. RESULTS: Regarding the clinical characteristics, the history of previous pancreatitis was distinguished in group with mass-forming pancreatitis. Incidence of jaundice was higher in the group with adenocarcinoma than in the mass-forming pancreatitis group. For laboratory results, CA19-9 level and alkaline phosphatase level were significantly elevated in the malignant group. Findings such as hyperattenuation on portal venous phase of CT scans and gradual tapering stricture on pancreatogram were differential diagnostic markers between the two groups. A portion of patients with mass-forming pancreatitis demonstrated the pathologic characteristics of autoimmune pancreatitis. CONCLUSIONS: Our 9-year experience suggests that imaging findings such as attenuation pattern on the delayed phase of CT scan and tapering pattern of pancreatic ductal stricture on pancreatogram can help to differentiate mass-forming pancreatitis from early-stage pancreatic adenocarcinoma.</P>
Lee, Youn-Sun,Choi, Heon-Kyo,Yoo, Jae-Myung,Choi, Kyong-Mi,Lee, Yong-Moon,Oh, Sei-Kwan,Kim, Tack-Joong,Yun, Yeo-Pyo,Hong, Jin-Tae,Okino, Nozomu,Ito, Makoto,Yoo, Hwan-Soo The Korean Society of Toxicogenomics and Toxicopro 2007 Molecular & cellular toxicology Vol.3 No.4
Ceramide is involved in cell death as a lipid mediator of stress responses. In this study, we developed an improved method of ceramide quantification based on added synthetic ceramide and thin layer chromatography (TLC) separation, and applied to biological samples. Lipids were extracted from samples spiked with N-oleoyl-D-erythro-sphingosine ($C_{17}$ ceramide) as an internal standard. Ceramide was resolved by TLC, complexed with fatty-acidfree bovine serum albumin (BSA), and deacylated by ceramidase (CDase). The released sphingosine was derivatized with o-phthalaldehyde (OPA) and measured by high performance liquid chromatography (HPLC). The limit of detection for ceramide was about 1-2 pmol and the lower limit of quantification was 5 pmol. Ceramide recovery was approximately 86-93%. Ceramide concentrations were determined in biological samples including cultured cells, mouse tissues, and mouse and human plasma. TLC separation of ceramide provides HPLC chromatogram with a clean background without any interfering peaks and the enhanced solubility of ceramide by BSAceramide complex leads to the increased deacylation of ceramide. The use of an internal standard for the determination of ceramide concentration in these samples provides an accurate and reproducible analytical method, and this method can be applicable to diverse biological samples.
CD30 활성화에 의한 호산구 자멸사에서 caspase-9 의 매개작용
이혜진 ( Hye Jin Lee ),이근영 ( Keun Young Lee ),김유진 ( Yoo Jin Kim ),장필상 ( Pil Sang Jang ),윤종서 ( Jong Seo Yoon ),김현희 ( Hyun Hee Kim ),고영률 ( Young Yull Koh ),김진택 ( Jin Tack Kim ),이준성 ( Joon Sung Lee ) 대한소아알레르기호흡기학회(구 대한소아알레르기 및 호흡기학회) 2011 소아알레르기 및 호흡기학회지 Vol.21 No.2
Purpose: Although CD30 is known to be expressed more on eosinophils undergoing apoptosis, it is still not known how CD30 activation leads to eosinophil apoptosis. In this study, we evaluated whether ligation of CD30 incites apoptosis and investigated whether the mechanisms of CD30 induced eosinophil apoptosis are dependent on caspase activation. Methods: We drew 90 mL of peripheral blood from healthy donors and then purified eosinophils using a MACS system. Expression of CD30 on eosinophils was measured, and eosinophils were cultured in wells pretreated with anti-CD30 mAb, isotype control immunoglobulin G1, interleukin (IL)-5, and dexamethasone in Roswell Park Memorial Institute 1640 media supplemented with 10% fetal bovine serum. Their rates of apoptosis were then compared using flow cytometry. To evaluate whether caspase-9 is involved in CD30-induced eosinophil apoptosis, the apoptotic rate was evaluated after the addition of caspase-9 inhibitor. The expression of procaspase-9 was also measured using Western blot. Results: Expression of CD30 molecules on eosinophils increased steadily as the culture time lapse. The apoptotic rates of eosinophils cultured in the presence of anti-CD30 mAb were significantly increased to 29.1±6.1% and 47.3±4.7% compared to 17.1±6.7% and 29.4±9.2% of the control at 4 and 24 hours, respectively (both P<0.05). The apoptotic rates of eosinophils treated with anti-CD30 mAb were even faster than those of eosinophils treated with dexamethasone, and the mAb also suppressed the IL-5-induced enhancing effect of eosinophil survival. Caspase-9 inhibitor suppressed mAb induced eosinophil apoptosis from 54.8±6.9% and 71.5±11.6% to 24.5±6.0% and 47.8±11.4% at 18 and 36 hours, respectively (both P<0.001). We also demonstrated that the expression of procaspase-9 with mAb was diminished compared to that of the control and of IL-5. Conclusion: This study showed CD30 activation enhances eosinophil apoptosis, and the effect is mediated by caspase-9 activation. [Pediatr Allergy Respir Dis(Korea) 2011;21:115-122]