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Outcome of ALPPS for Hepatocellular Carcinoma
( Albert Chan ),( Kenneth Chok ),( Jeff Dai ),( Chung Mau Lo ),( Wong Hoi She ) 대한간학회 2017 춘·추계 학술대회 (KASL) Vol.2017 No.1
Aims: ALPPS has changed the management of patients with inadequate future liver remnant (FLR) contemplating for major hepatectomy in colorectal metastasis but its efficacy for hepatocellular carcinoma (HCC) in chronic hepatitis/cirrhosis is not substantiated. We hereby reported our experience of ALPPS in hepatitis-related HCC. Methods: From October 2013 - November 2016, patients with Child A cirrhosis and FLR < 35% of estimated total liver volume (ESLV) were selected for ALPPS. Portal haemodynamic was studied. Postoperative outcome was compared with portal vein embolization (PVE, n=56) matched for age, liver function and tumor characteristics Results: 36 patients (hepatitis B, n=35; hepatitis C, n=1) underwent ALPPS. Preoperative FLR/ESLV was 24.6% and ICG value was 12.8%. Portal flow to FLR increased from 200.0ml/min to 737.5ml/min after ALPPS. ALPPS induced FLR volume gain by 52.7% in 6 days (post-ALPPS FLR/ESLV = 37.6%) and all patients received stage II operation (right hepatectomy, n =18, extended right hepatectomy, n=11, right trisectionectomy, n=6). The time to hepatectomy for ALPPS and PVE were 7 and 48 days, respectively (p<0.001). ALPPS induced greater FLR hypertrophy than PVE (daily FLR gain: 6.0% vs. 0.8%, p<0.001) without increased morbidity (30.4% vs. 32.1%, p=0.978) and mortality (8.6% vs. 7.1%, p=0.801). 1-year tumor recurrence rate for ALPPS and PVE were similar (TNM I/II: 0% vs. 20.5%, p=0.433; TNM III: 53.8% vs. 52.2%, p=1.000 respectively). Conclusions: ALPPS induced greater FLR hypertrophy than PVE in chronic liver disease without increased postoperative risk. The entire treatment course was effectively completed within one hospitalization
Ivan Ho Yuen Pun,Dessy Chan,Sau Hing Chan,Po Yee Chung,Yuanyuan Zhou,Simon Law,Alfred King Yin Lam,Chung Hin Chui,Albert Sun Chi Chan,Kim Hung Lam,Johnny Cheuk On Tang 대한암학회 2017 Cancer Research and Treatment Vol.49 No.1
Purpose 83b1 is a novel quinoline derivative that has been shown to inhibit cancer growth in human esophageal squamous cell carcinoma (ESCC). This study was conducted to comprehensively evaluate the cytotoxic effects of 83b1 on a series of ESCC cell lines and investigate the mechanisms by which 83b1 suppresses cancer growth based on molecular docking analysis. Materials and Methods A series of ESCC and nontumor immortalized cell lines were exposed to 83b1 and cisplatin (CDDP) in a dose-dependent manner, and the cytotoxicity was examined by a MTS assay kit. Prediction of the molecular targets of 83b1 was conducted by molecular docking analysis. Expression of cyclooxygenase 2 (COX-2) mRNA and COX-2–derived prostaglandin E2 (PGE2) were measured by quantitative real-time polymerase chain reaction and enzymelinked immuno-sorbent assay, respectively. In vivo anti-tumor effect was determined using a nude mice xenografted model transplanted with an ESCC cell line, KYSE-450. Results 83b1 showed the significant anti-cancer effects on all ESCC cell lines compared to CDDP; however, 83b1 revealed much lower toxic effects on non-tumor cell lines than CDDP. The predicted molecular target of 83b1 is peroxisome proliferator-activated receptor delta (PPAR), which is a widely known oncoprotein. Additionally the expression of COX-2 mRNA and COX-2–derived PGE2 were down-regulated by 83b1 in a dose-dependent manner in ESCC cell lines. Furthermore, 83b1 was shown to significantly reduce the tumor size in nude mice xenograft. Conclusion The results of this study suggest that the potential anti-cancer effects of 83b1 on human esophageal cancers occur through the possible oncotarget, PPAR, and down-regulation of the cancer related genes and molecules.
Alberts Rudi,Chan Sze Chun,Meng Qian-Fang,He Shan,Rao Lang,Liu Xindong,Zhang Yongliang 대한면역학회 2022 Immune Network Vol.22 No.3
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), has spread over the world causing a pandemic which is still ongoing since its emergence in late 2019. A great amount of effort has been devoted to understanding the pathogenesis of COVID-19 with the hope of developing better therapeutic strategies. Transcriptome analysis using technologies such as RNA sequencing became a commonly used approach in study of host immune responses to SARS-CoV-2. Although substantial amount of information can be gathered from transcriptome analysis, different analysis tools used in these studies may lead to conclusions that differ dramatically from each other. Here, we re-analyzed four RNA-sequencing datasets of COVID-19 samples including human bronchoalveolar lavage fluid, nasopharyngeal swabs, lung biopsy and hACE2 transgenic mice using the same standardized method. The results showed that common features of COVID-19 include upregulation of chemokines including CCL2, CXCL1, and CXCL10, inflammatory cytokine IL-1β and alarmin S100A8/S100A9, which are associated with dysregulated innate immunity marked by abundant neutrophil and mast cell accumulation. Downregulation of chemokine receptor genes that are associated with impaired adaptive immunity such as lymphopenia is another common feather of COVID-19 observed. In addition, a few interferon-stimulated genes but no type I IFN genes were identified to be enriched in COVID-19 samples compared to their respective control in these datasets. These features are in line with results from single-cell RNA sequencing studies in the field. Therefore, our re-analysis of the RNA-seq datasets revealed common features of dysregulated immune responses to SARS-CoV-2 and shed light to the pathogenesis of COVID-19.
Lee, Albert S.,Lee, Jin Hong,Lee, Jong-Chan,Hong, Soon Man,Hwang, Seung Sang,Koo, Chong Min American Scientific Publishers 2017 Journal of Nanoscience and Nanotechnology Vol.17 No.5
<P>The compatibility of diacrylate terminated polyethylene glycol-block-polydimethylsiloxane-block-polyethylene glycol was examined with an ionic liquid solution, 1 M LiTFSI in N-butyl-N-methylpyrrolidinium bis(trifluoromethylsulfonyl)imide, and through mild UV-curing, hybrid gel polymer electrolytes were fabricated for lithium ion battery application. Obtained hybrid gel polymer electrolytes exhibited good ionic conductivity, electrochemical stability, thermal stability, and mechanical pliancy and the polyethylene glycol domains functioned to increase the ionic dissociation to improve ion conduction compared with gel polymer electrolytes fabricated with a conventional organic crosslinker. Lithium ion battery cell tests with these hybrid gel polymer electrolytes revealed that these hybrid gel polymer electrolytes hold promise as next generation electrolytes.</P>
Anti-Inflammatory and Antiatherogenic Role of BMP Receptor II in Endothelial Cells
Kim, Chan Woo,Song, Hannah,Kumar, Sandeep,Nam, Douglas,Kwon, Hyuk Sang,Chang, Kyung Hwa,Son, Dong Ju,Kang, Dong-Won,Brodie, Seth A.,Weiss, Daiana,Vega, J. David,Alberts-Grill, Noah,Griendling, Kathy,T American Heart Association, Inc. 2013 Arteriosclerosis, thrombosis, and vascular biology Vol.33 No.6
<P><B>Objective—</B></P><P>Atherosclerosis is an inflammatory disease with multiple underlying metabolic and physical risk factors. Bone morphogenic protein 4 (BMP4) expression is increased in endothelium in atherosclerosis-prone regions and is known to induce endothelial inflammation, endothelial dysfunction, and hypertension. BMP actions are mediated by 2 different types of BMP receptors (BMPRI and BMPRII). Here, we show a surprising finding that loss of BMPRII expression causes endothelial inflammation and atherosclerosis.</P><P><B>Approach and Results—</B></P><P>Using BMPRII siRNA and BMPRII<SUP>+/−</SUP> mice, we found that specific knockdown of BMPRII, but not other BMP receptors (Alk1, Alk2, Alk3, Alk6, ActRIIa, and ActRIIb), induced endothelial inflammation in a ligand-independent manner by mechanisms mediated by reactive oxygen species, nuclear factor-KappaB, and reduced nicotinamide adenine dinucleotide phosphate oxidases. Further, BMPRII<SUP>+/−</SUP>ApoE<SUP>−/−</SUP> mice developed accelerated atherosclerosis compared with BMPRII<SUP>+/+</SUP>ApoE<SUP>−/−</SUP> mice. Interestingly, we found that multiple proatherogenic stimuli, such as hypercholesterolemia, disturbed flow, prohypertensive angiotensin II, and the proinflammatory cytokine (tumor necrosis factor-α), downregulated BMPRII expression in endothelium, whereas antiatherogenic stimuli, such as stable flow and statin treatment, upregulated its expression in vivo and in vitro. Moreover, BMPRII expression was significantly diminished in human coronary advanced atherosclerotic lesions. Also, we were able to rescue the endothelial inflammation induced by BMPRII knockdown by overexpressing the BMPRII wild type, but not by the BMPRII short form lacking the carboxyl-terminal tail region.</P><P><B>Conclusions—</B></P><P>These results suggest that BMPRII is a critical, anti-inflammatory, and antiatherogenic protein that is commonly targeted by multiple pro- and antiatherogenic factors. BMPRII may be used as a novel diagnostic and therapeutic target in atherosclerosis.</P>
Darren Chua,Albert Low,Yexin Koh,Brian Goh,Peng Chung Cheow,Juinn Har Kam,Jin Yao Teo,Ek Khoon Tan,Alexander Chung,London Lucien Ooi,Chung Yip Chan,Ser Yee Lee 한국간담췌외과학회 2018 Annals of hepato-biliary-pancreatic surgery Vol.22 No.3
Backgrounds/Aims: Hilar cholangiocarcinomas (HCCAs) are tumors that involve the biliary confluence; at present, radical surgery offers the only chance of long-term survival, but this can be challenging given the complexity of the hilar anatomy. Blumgart and Jarnagin described a preoperative staging system that incorporates the effect of local tumor extent and its impact on adjacent structures and that has been demonstrated to correlate better with actual surgical resectability. The primary aim of this study is to describe the correlation between preoperative Blumgart-Jarnagin staging and its correlation with surgical resectability. Methods: Patients who underwent surgical resection for hilar cholangiocarcinoma at Singapore General Hospital between January 1, 2002, and January 1, 2013, were identified from a prospectively maintained institutional database. All patients were staged based on the criteria described by Blumgart and Jarnagin. Correlation with surgical resectability was then determined. Results: A total of 19 patients were identified. Overall resectability was 57.8% (n=11). Patients with Blumgart-Jarnagin stage T1 had the highest rates of respectability at 80%; patients with stage T2 and T3 disease had resectability rates of 25% and 40% respectively. Median overall survival was 13.6 months. Conclusions: The Blumgart-Jarnagin staging system is useful for predicting tumor respectability in HCCA.