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SW Banyan-Data Manipulator Network를 위한 制御 알고리즘
李楨賢,李文儀 경기대학교부설 산업기술종합연구소 1986 산업기술종합연구소 논문집 Vol.2 No.-
In this paper, the architecture of SW Banyan-Data manipulator network is studied, and a control algorithm for this network is proposed.
유현아,김은영,서민지,정은,조민정,오현진,장지혜,박지찬,이정의,박석영 이화여자대학교 의과학연구소 2014 EMJ (Ewha medical journal) Vol.37 No.2
Gastric metastasis from breast cancer is rare and only six cases have been reported in Korea. Colon metastasis is more rare than gastric metastasis. We report a 63-year-old woman with gastric and colon metastases of invasive lobular carcinoma of breast. She was diagnosed as right breast cancer, received right modified radical mastectomy 10 years ago and has been treated with chemotherapy and hormone therapy. Investigating for melena and a small caliber of stool, we found gastric and colon metastases. The diagnosis of metastatic breast cancer was made through gross pathologic and immunohistochemistry staining. We report a case with gastric and colon metastases from breast cancer and a review of the associated six case reports in Korea.
Dual specificity phosphatase 6 as a predictor of invasiveness in papillary thyroid cancer.
Lee, Jung Uee,Huang, Songmei,Lee, Min Hee,Lee, Seong Eun,Ryu, Min Jeong,Kim, Soung Jung,Kim, Yong Kyung,Kim, Seul Young,Joung, Kyong Hye,Kim, Jin Man,Shong, Minho,Jo, Young Suk Scandinavian University Press 2012 European journal of endocrinology Vol.167 No.1
<P>The genetic mutations causing the constitutive activation of MEK/ERK have been regarded as an initiating factor in papillary thyroid carcinoma (PTC). The ERK-specific dual specificity phosphatase 6 (DUSP6) is part of the ERK-dependent transcriptional output. Therefore, the coordinated regulation of the activities of ERK kinases and DUSP6 may need to be reestablished to make new balances in PTC.</P>
Thyroid dysfunction associated with follicular cell steatosis in obese male mice and humans.
Lee, Min Hee,Lee, Jung Uee,Joung, Kyong Hye,Kim, Yong Kyung,Ryu, Min Jeong,Lee, Seong Eun,Kim, Soung Jung,Chung, Hyo Kyun,Choi, Min Jeong,Chang, Joon Young,Lee, Sang-Hee,Kweon, Gi Ryang,Kim, Hyun Jin The Endocrine Society 2015 Endocrinology Vol.156 No.3
<P>Adult thyroid dysfunction is a common endocrine disorder associated with an increased risk of cardiovascular disease and mortality. A recent epidemiologic study revealed a link between obesity and increased prevalence of hypothyroidism. It is conceivable that excessive adiposity in obesity might lead to expansion of the interfollicular adipose (IFA) depot or steatosis in thyroid follicular cells (thyroid steatosis, TS). In this study, we investigated the morphological and functional changes in thyroid glands of obese humans and animal models, diet-induced obese (DIO), ob/ob, and db/db mice. Expanded IFA depot and TS were observed in obese patients. Furthermore, DIO mice showed increased expression of lipogenesis-regulation genes, such as sterol regulatory element binding protein 1 (SREBP-1), peroxisome proliferator-activated receptor γ (PPARγ), acetyl coenzyme A carboxylase (ACC), and fatty acid synthetase (FASN) in the thyroid gland. Steatosis and ultrastructural changes, including distension of the endoplasmic reticulum (ER) and mitochondrial distortion in thyroid follicular cells, were uniformly observed in DIO mice and genetically obese mouse models, ob/ob and db/db mice. Obese mice displayed a variable degree of primary thyroid hypofunction, which was not corrected by PPARγ agonist administration. We propose that systemically increased adiposity is associated with characteristic IFA depots and TS and may cause or influence the development of primary thyroid failure.</P>
( Jung Uee Lee ),( Hae Joung Sul ),( Ji Woong Son ) 대한결핵 및 호흡기학회 2012 Tuberculosis and Respiratory Diseases Vol.73 No.1
Background: While qualitative analysis of methylation has been reviewed, the quantitative analysis of methylation has rarely been studied. We evaluated the methylation status of CDKN2A, RARβ, and RASSF1A promoter regions in non-small cell lung carcinomas (NSCLCs) by using pyrosequencing. Then, we evaluated the association between methylation at the promoter regions of these tumor suppressor genes and the clinicopathological parameters of the NSCLCs. Methods: We collected tumor tissues from a total of 53 patients with NSCLCs and analyzed the methylation level of the CDKN2A, RARβ, and RASSF1A promoter regions by using pyrosequencing. In addition, we investigated the correlation between the hypermethylation of CDKN2A and the loss of p16INK4A immunoexpression. Results: Hypermethylation of CDKN2A, RARβ, and RASSF1A promoter regions were 16 (30.2%), 22 (41.5%), and 21 tumors (39.6%), respectively. The incidence of hypermethylation at the CDKN2A promoter in the tumors was higher in undifferentiated large cell carcinomas than in other subtypes (p=0.002). Hyperrmethylation of CDKN2A was significantly associated with p16INK4A immunoexpression loss (p=0.045). With regard to the clinicopathological characteristics of NSCLC, certain histopathological subtypes were found to be strongly associated with the loss of p16INK4A immunoexpression (p=0.016). Squamous cell carcinoma and undifferentiated large cell carcinoma showed p16INK4A immunoexpression loss more frequently. The Kaplan-Meier survival curves analysis showed that methylation level and patient survival were barely related to one another. Conclusion: We quantitatively analyzed the promoter methylation status by using pyrosequencing. We showed a significant correlation between CDKN2A hypermethylation and p16INK4A immunoexpression loss.
Lee, Jung Uee,Sul, Hae Joung,Son, Ji Woong The Korean Academy of Tuberculosis and Respiratory 2012 Tuberculosis and Respiratory Diseases Vol.73 No.1
Background: While qualitative analysis of methylation has been reviewed, the quantitative analysis of methylation has rarely been studied. We evaluated the methylation status of CDKN2A, $RAR{\beta}$, and RASSF1A promoter regions in non-small cell lung carcinomas (NSCLCs) by using pyrosequencing. Then, we evaluated the association between methylation at the promoter regions of these tumor suppressor genes and the clinicopathological parameters of the NSCLCs. Methods: We collected tumor tissues from a total of 53 patients with NSCLCs and analyzed the methylation level of the CDKN2A, $RAR{\beta}$, and RASSF1A promoter regions by using pyrosequencing. In addition, we investigated the correlation between the hypermethylation of CDKN2A and the loss of $p16^{INK4A}$ immunoexpression. Results: Hypermethylation of CDKN2A, $RAR{\beta}$, and RASSF1A promoter regions were 16 (30.2%), 22 (41.5%), and 21 tumors (39.6%), respectively. The incidence of hypermethylation at the CDKN2A promoter in the tumors was higher in undifferentiated large cell carcinomas than in other subtypes (p=0.002). Hyperrmethylation of CDKN2A was significantly associated with $p16^{INK4A}$ immunoexpression loss (p=0.045). With regard to the clinicopathological characteristics of NSCLC, certain histopathological subtypes were found to be strongly associated with the loss of $p16^{INK4A}$ immunoexpression (p=0.016). Squamous cell carcinoma and undifferentiated large cell carcinoma showed $p16^{INK4A}$ immunoexpression loss more frequently. The Kaplan-Meier survival curves analysis showed that methylation level and patient survival were barely related to one another. Conclusion: We quantitatively analyzed the promoter methylation status by using pyrosequencing. We showed a significant correlation between CDKN2A hypermethylation and $p16^{INK4A}$ immunoexpression loss.