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Oncologic Outcome after 2 Stage Hepatectomy - Experience of Single Institution
( Sung Whan Cha ),( Dai Hoon Han ),( Gi Hong Choi ),( Jin Sub Choi ) 대한간학회 2017 춘·추계 학술대회 (KASL) Vol.2017 No.1
Aims: To evaluate the oncologic outcome after 2 stage hepatectomy for colorectal liver metastasis. Methods: From January 2010 to December 2016, 23 patients who underwent 2 stage hepatectomy for colorectal liver metastasis were enrolled. Perioperative outcome and oncologic outcome were reviewed retrospectively. Results: Median interval between 1st hepatectomy and 2nd hepatectomy was 27.9±12.1 days, and postoperative hospital stay after 2nd hepatectomy was 16±9.25 days. Complication after 2nd hepatectomy was reported in grade II 7 cases, grade III 5 cases and grade V 1 case. For portal vein ligation, percutaneous portal vein embolization was done in 12 patients, intraoperatively selective portal vein ligation was done in 5 patients and ALPPS was done in 6 patients. Median disease free survival and overall survival were reported 5.25 months and 32.25 months respectively. 14 patients had early recurrence less then 6 months after 2nd hepatectomy. Conclusions: 2 stage hepatectomy can be performed safely and aslo can give chance for long-term survival for colorectal liver metastasis. Further study is required for prognostic factor for recurrence as there is high possibility of early recurrence
( Sung Woo Cho ),( Na Ri Park ),( Jung Hoon Cha ),( Jeong Won Jang ),( Jong Young Choi ),( Seung Kew Yoon ),( Si Hyun Bae ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: CD44 have known as important modulators of epithelial-mesenchymal transition (EMT) together with transforming growth factor beta1 (TGF-β1). Moreover, CD44 and TGF-β1 double positive more enhanced cancer stem cell characteristics acquisition, EMT, and metastasis. In cancer, miRNAs functions as tumor suppressors or oncogenes. This study aimed to investigate the identify microRNAs regulating the EMT with CD44/ TGF-β1 in HCC cells. Methods: We sorted CD44<sup>-</sup> and CD44<sup>+</sup> liver cancer stem cells by fluorescence-activated cell sorting (FACs) in TGF-β1-positive SNU-368 cells and TGF-β1-negative SNU-354 cells. The miRNA profiles of CD44<sup>-</sup> and CD44<sup>+</sup> HCC cells were analyzed by next-generation sequencing (NGS). To investigate synergy effect of CD44 and TGF-β1, we induced EMT by TGF-β1 treatment or inhibited EMT by TGF-β1 inhibitors. The expression level of mRNA and protein were detected by quantitative real-time PCR (qRT-PCR) and western blot. Results: miRNA NGS array data were compared among CD44 or TGF-β1 single expression HCC cells and CD44/TGF-β1 double positive HCC cells. The results showed that four miRNAs (miR-96-5p, miR-221-5p, miR-186-3p and miR-152-3p) were up-regulated and two miRNAs (miR-296-3p, miR-10a-5p) was down-regulated in CD44<sup>+</sup>/TGF-β1<sup>+</sup> cells than an expression of either one alone. These results were confirmed by qRT-PCR. TGF-β1-stimulated SNU-354 (CD44+/TGF-β1<sup>+</sup>) cells up-regulated three miRNAs (miR-96-5p, miR-221-5p, miR-186-3p) than SNU-354 (CD44<sup>+</sup>/TGF-β1<sup>-</sup>) cells and also, down-regulated the two miRNAs (miR-296-3p, miR-10a-5p). Inhibition of TGF-β1 in SNU-368 cells reduced miR-221-5p and increased miR-296-3p. Furthermore, TGF-β1-stimulated SNU-354 (CD44<sup>+</sup>/TGF-β1<sup>+</sup>) cells induced EMT and TGF-β1 inhibitor-treated SNU-368 (CD44<sup>+</sup>/ TGF-β1<sup>-</sup>) cells inhibited EMT. Overexpression of miR-221-5p in SNU-354 (CD44<sup>+</sup>/TGF-β1<sup>-</sup>) cells exhibited lower E-cadherin and higher β-catenin. Next, the loss of miR-221-5p in SNU-368 (CD44<sup>+</sup>/TGF-β1<sup>+</sup>) cells showed increased E-cadherin. Conclusions: We identified CD44/TGF-β1-related miRNAs and confirmed regulation of EMT by miRNAs in HCC cells. The results would suggest a possible application that CD44/TGF-β1- regulated miRNAs may serve as specific biomarkers and therapeutic targets for hepatocellular carcinoma.
IoT Open-Source and AI based Automatic Door Lock Access Control Solution
Sung Hoon Yoon,Kil Soo Lee,Jae Sang Cha,Vinayagam Mariappan,Ko Eun Young,Deok Gun Woo,Jeong Uk Kim 한국인터넷방송통신학회 2020 International Journal of Internet, Broadcasting an Vol.12 No.2
Recently, there was an increasing demand for an integrated access control system which is capable of user recognition, door control, and facility operations control for smart buildings automation. The market available door lock access control solutions need to be improved from the current level security of door locks operations where security is compromised when a password or digital keys are exposed to the strangers. At present, the access control system solution providers focusing on developing an automatic access control system using (RF) based technologies like bluetooth, WiFi, etc. All the existing automatic door access control technologies required an additional hardware interface and always vulnerable security threads. This paper proposes the user identification and authentication solution for automatic door lock control operations using camera based visible light communication (VLC) technology. This proposed approach use the cameras installed in building facility, user smart devices and IoT open source controller based LED light sensors installed in buildings infrastructure. The building facility installed IoT LED light sensors transmit the authorized user and facility information color grid code and the smart device camera decode the user informations and verify with stored user information then indicate the authentication status to the user and send authentication acknowledgement to facility door lock integrated camera to control the door lock operations. The camera based VLC receiver uses the artificial intelligence (AI) methods to decode VLC data to improve the VLC performance. This paper implements the testbed model using IoT open-source based LED light sensor with CCTV camera and user smartphone devices. The experiment results are verified with custom made convolutional neural network (CNN) based AI techniques for VLC deciding method on smart devices and PC based CCTV monitoring solutions. The archived experiment results confirm that proposed door access control solution is effective and robust for automatic door access control.
Cha, Hoon-Suk,Bae, Eun-Kyung,Ahn, Joong-Kyong,Lee, Jae-Joon,Ahn, Kwang-Sung,Koh, Eun-Mi Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.6
Inadequate apoptosis contributes to synovial hyperplasia in rheumatoid arthritis (RA). Recent study shows that low expression of Puma might be partially responsible for the decreased apoptosis of fibroblast-like synoviocytes (FLS). Slug, a highly conserved zinc finger transcriptional repressor, is known to antagonize apoptosis of hematopoietic progenitor cells by repressing Puma transactivation. In this study, we examined the expression and function of Slug in RA FLS. Slug mRNA expression was measured in the synovial tissue (ST) and FLS obtained from RA and osteoarthritis patients. Slug and Puma mRNA expression in FLS by apoptotic stimuli were measured by real-time PCR analysis. FLS were transfected with control siRNA or Slug siRNA. Apoptosis was quantified by trypan blue exclusion, DNA fragmentation and caspase-3 assay. RA ST expressed higher level of Slug mRNA compared with osteoarthritis ST. Slug was significantly induced by hydrogen peroxide ($H_2O_2$) but not by exogenous p53 in RA FLS. Puma induction by $H_2O_2$ stimulation was significantly higher in Slug siRNA-transfected FLS compared with control siRNA-transfected FLS. After $H_2O_2$ stimulation, viable cell number was significantly lower in Slug siRNA-transfected FLS compared with control siRNA-transfected FLS. Apoptosis enhancing effect of Slug siRNA was further confirmed by ELISA that detects cytoplasmic histone-associated DNA fragments and caspase-3 assay. These data demonstrate that Slug is overexpressed in RA ST and that suppression of Slug gene facilitates apoptosis of FLS by increasing Puma transactivation. Slug may therefore represent a potential therapeutic target in RA.