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- 저자 : Sung-Woo Bae (검색결과 3,648 건)
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Bae, Doo Ri,Lee, You-Jin,Lee, Sung Woo,Han, Young-Kyu,Yoon, Jae-Sik,Lee, Ji-Hyun,Lee, Sang-Gil,Chang, Ki Soo,Yi, Gi-Ra,Lee, Gaehang American Scientific Publishers 2014 Journal of nanoscience and nanotechnology Vol.14 No.12
<P>Electro-sterically stabilized gold suspensions were employed in a colorimetric system for the detection of strong acid in water. Using oleyamine and oleic acid as steric stabilizer in 1,2-dichlorobenzene, hydrophobic gold nanoparticles were first synthesized by a reduction reaction of gold salts and were then transferred into water with a cationic surfactant. When the hydrochlo- ric acid solution higher than critical concentration was injected, particles were quickly aggregated and precipitated, creating a clear solution from the colored suspension. The particles were stable against chemical etching by corrosive ion such as chloride. Critical concentration was dependent of the size and concentration of the particles. The minimum concentration of dramatic color change was at 5 ppm level of hydrochloric acid, in which the largest colloidal gold nanoparticles (54 nm) were used. Furthermore, because of their steric repulsive soft layer on particles, particles could be reused for further detection experiments after regeneration by the simple pH-neutralization and washing process.</P>
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Bae, Hyun Jin,Eun, Jung Woo,Noh, Ji Heon,Kim, Jeong Kyu,Jung, Kwang Hwa,Xie, Hong Jian,Park, Won Sang,Lee, Jung Young,Nam, Suk Woo National Hellenic Research Foundation 2009 ONCOLOGY REPORTS Vol.22 No.3
<P>The transforming growth factor receptor III (TGFbetaRIII) is the most abundant and essential TGF-beta binding protein that functions as a co-receptor with other receptors in TGF-beta signaling. In earlier studies, expression of TGFbetaRIII was reported to be decreased in a variety of human cancers. Functional assessment of TGFbetaRIII was performed in many previously studied cancers but not in hepatocellular carcinoma. Therefore, in this study, we investigated the expression and genetic alterations of TGFbetaRIII in hepatocellular carcinoma (HCC) by quantitative real-time PCR (qRT-PCR) and single-strand conformation polymorphism (SSCP) analysis. The qRT-PCR showed down-regulation of TGFbetaRIII in the tumor samples. To investigate whether genetic alterations mediated decreased expression of TGFbetaRIII, we performed mutation analysis of 67 human HCC tissues by SSCP and direct sequencing. We found five previously reported and one novel single nucleotide polymorphisms in exons 2, 3, 5, 13 and 14, but no mutations were detected. These polymorphisms were not associated with amino acid changes except for a base change found in exon 2 (TCC-->TTC, S15F). The loss of heterozygosity (LOH) analysis performed on 10 tumors and corresponding normal pairs, showed a low rate of LOH (2/10). The results of this study suggest that TGFbetaRIII is transcriptionally down-regulated in hepatocellular carcinoma. In addition, genetic alterations did not appear to be associated with the reduced expression level of TGFbetaRIII. To clarify the role of TGFbetaRIII in hepatocellular tumor development and progression, functional analysis is needed in future studies.</P>
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Micropunch grafting for hypopigmented burn scar
( Sung Hye Eun ),( Han Mi Jung ),( Soo Hyung Kim ),( Ro Woo Lee ),( Hyun Jeong Ju ),( Ji Hae Lee ),( Gyong Moon Kim ),( Jung Min Bae ) 대한피부과학회 2019 대한피부과학회 학술발표대회집 Vol.71 No.1
Punch grafting has been used to treat refractory vitiligo; but the principal limitations were the lengthy treatment time and resulting cobblestone appearance. Recently, motorized 0.8-mm micropunch grafting was introduced; this overcomes the disadvantages of the conventional approach. Micropunch grafting could be conveniently and successfully used to treat not only vitiligo, but also various intractable depigmentation skin disorders including hypopigmented burn scars. A 57-year-old male presented with a hypopigmented scar on his left shoulder. The scar developed after he had personally removed a tattoo using vinegar 10 years prior. Thereafter, he had undergone excimer laser treatment for 12 months at a clinic, but the depigmentation did not improve. We performed micropunch grafting using a stainless-steel punch 0.8 mm in diameter loaded into the handpiece of a micromotor (SST-C1; Ilooda Co., Suwon, Korea). First, after local anesthesia, the full-thickness skin was removed to create chambers for planting grafts using the instrument at the recipient site. Then, micropunch grafts were harvested from the post-auricular region (the donor site). Next, the grafts were placed into the recipient chambers. Hydrocolloid and Steri-Strip dressings were applied to the donor and recipient sites, respectively. One week later, twice weekly, 308-nm excimer laser treatment was initiated, and complete repigmentation was attained by 3 months.
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( Sung Woo Cho ),( Jung Hoon Cha ),( Na Ri Park ),( Won Hee Hur ),( Pill Soo Sung ),( Jong Young Choi ),( Seung Kew Yoon ),( Si Hyun Bae ),( Hee Chul Nam ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: Non-alcoholic fatty liver disease (NAFLD) is a metabolic- related disorder ranging from simple steatosis to more severe forms, but the exact mechanism of progression remains unknown. MicroRNAs(miR), a class of small noncoding RNAs, are implicated in controlling a variety of biological processes. The aim of this study is to investigate the regulatory and protective role of miR-22-3p in NAFLD progression. Methods: Both in vitro and in vivo models of NAFLD were generated by treating HepG2 and Huh-7 cells with palmitic acid (PA) and by feeding mice a high-fat diet (HFD), respectively. HE and Oil Red O staining were used to examine liver tissue morphology and lipid deposition, respectively. qRT-PCR (quantitative real time polymerase chain reaction) was used for investigate expression of miR, SIRT1, and proteins involved in lipogenesis Results: HFD-mice hepatic tissues and PA-treated HepG2 and Huh-7 cells presented excess lipid production. Both in vitro and in vivo NAFLD model displayed decreased miR-22-3p and SIRT1 expression as evidenced by qRT-PCR. Overexpression of miR-22-3p induced downregulation of FAS, PPAR gamma and SREBP-1c via upregulation of SIRT1 expression. Reduction of hepatic lipid accumulation was observed by Oil red O staining. Conclusions: In this study, miR-22-3p had a role in ameliorating hepatic lipogenesis by regulation of SIRT1 signal pathway in NAFLD model. The overexpressed miR-22-3p protects hepatocytes from lipid metabolism and suppresses hepatic lipogenesis, suggesting as a potential target for the therapeutic strategy of NAFLD.
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Bae, Woo-Chul,Lee, Han-Ki,Choe, Young-Chool,Jahng, Deok-Jin,Lee, Sang-Hee,Kim, Sang-Jin,Lee, Jung-Hyun,Jeong, Byeong-Chul The Microbiological Society of Korea 2005 The journal of microbiology Vol.43 No.1
A soluble Cr(VI) reductase was purified from the cytoplasm of Escherichia coli ATCC 33456. The molecular mass was estimated to be 84 and 42 kDa by gel filtration and SDS-polyacrylamide gel electrophoresis, respectively, indicating a dimeric structure. The pI was 4.66, and optimal enzyme activity was obtained at pH 6.5 and $37^{\circ}C$. The most stable condition existed at pH 7.0. The purified enzyme used both NADPH and NADH as electron donors for Cr(VI) reduction, while NADPH was the better, conferring 61% higher activity than NADH. The $K_m$ values for NADPH and NADH were determined to be 47.5 and 17.2 umol, and the $V_max$ values 322.2 and 130.7 umol Cr(VI) $min^{-1}mg^{-1}$ protein, respectively. The activity was strongly inhibited by N-ethylmalemide, $Ag^{2+},\;Cd^{2+},\;Hg^{2+}$, and $Zn^{2+}$. The antibody against the enzyme showed no immunological cross reaction with those of other Cr(VI) reducing strains.
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Bae, Woo Yong,Kim, Lee Suk,Hur, Dae Young,Jeong, Sung Wook,Kim, Jae Ryong The American Laryngological, Rhinological Otologic 2008 The Laryngoscope Vol.118 No.9
OBJECTIVES/HYPOTHESIS:: Hair cell loss results in the secondary loss of spiral ganglion neurons (SGNs), over a period of several weeks. The death of the SGNs themselves results from apoptosis. Previous studies have shown that several molecules are involved in the apoptosis of SGNs that occurred secondary to hair cell loss. However, the precise mechanism of apoptosis of the SGNs remains unclear. The aim of this study was to ascertain the secondary apoptosis of spiral ganglion cells induced by aminoglycoside and to investigate the role of the Fas–FasL signaling pathway using guinea pigs as an experimental animal model. STUDY DESIGN:: Laboratory study using experimental animals. METHODS:: Guinea pigs weighing 250 to 300 g (n = 21) from 3 to 4 weeks of age were used. Gentamicin (60 μL) was injected through a cochleostomy site on their left side. At 1 (n = 7), 2 (n = 7), and 3 (n = 7) weeks after gentamicin treatment, their cochleas were obtained from their temporal bone. Hematoxylin and eosin and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling staining were performed to observe apoptosis. To investigate the involvement of the Fas–FasL signaling pathway in the secondary apoptosis of SGNs, we performed reverse transcription-polymerase chain reaction (RT-PCR), western blotting, and immunohistochemistry. RESULTS:: A progressive loss of spiral ganglion cells with increasing time after gentamicin treatment was observed on light microscopic examination. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling staining demonstrated induction of apoptotic cell death in SGNs after gentamicin treatment. Expression of FasL increased over time after gentamicin treatment as determined by RT-PCR and western blotting. On immunohistochemical staining, we observed the localization of FasL in the SGNs. The proapoptotic molecules Bax and Bad were increased, but levels of the antiapoptotic molecule Bcl-2 were decreased at increasing survival times after gentamicin treatment on RT-PCR. The gentamicin-treated group displayed initial activation of caspase-8 and increased the cleavage of caspase-3, caspase-8, and PARP protein in a time-dependent manner. CONCLUSIONS:: The secondary apoptosis of SGNs could be a result of the apoptotic Fas–FasL signaling pathway. Blocking the Fas–FasL signaling pathway could be considered as a method for preventing secondary degeneration of SGNs, and further studies are needed to confirm this.
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Sang-Ho Jeong,Kyungsoo Bae,Chang-Youn Ha,Young-Joon Lee,Ok-Jae Lee,Woon-Tae Jung,Sang-Kyung Choi,Soon-Chan Hong,Eun-Jung Jung,Young-Tae Ju,Chi-Young Jeong,Woo-Song Ha 대한외과학회 2013 Annals of Surgical Treatment and Research(ASRT) Vol.84 No.2
Purpose: Before laparoscopic gastrectomy for gastric cancer can be planned, it is very important to know the precise location of the tumor. The aim of this study was to evaluate 3 methods of predicting the exact location of the tumor: preoperative gastrofibroscopy (GFS), preoperative computed tomography gastroscopy (CT), and intraoperative gastroscopy-guided laparoscopy (Lap). Methods: In this study, 15 patients were prospectively identified, and endoscopic clips were preoperatively placed on the proximal 1 cm of the tumor, at the angle on the greater curvature and opposite the angle on the greater curvature. The distances between the pylorus and the proximal tumor clip (PT), the angle clip (PA), the greater curvature clip (PG), and the gastroesophageal junction were measured by preoperative GFS, preoperative CT, intraoperative Lap, and visual inspection (Vis). Results: PT, PA, and PG values measured by preoperative GFS differed significantly from the Vis values (P 〈 0.01). However, preoperative CT measurements of PT, PA, and PG did not differ from the Vis values (P = 0.78, P = 0.48, and P = 0.53, respectively). Intraoperative Lap and Vis PT values differed by only 1.1 cm on an average (P = 0.10), but PA and PG values varied by 1.9 and 3.4 cm, respectively (P = 0.01 for both). Conclusion: Endoscopic clipping combined with preoperative CT gastroscopy is more useful than preoperative GFS for preoperatively predicting the location of early gastric cancers and will be helpful for planning laparoscopic gastrectomy.
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Fatty acid-CoA ligase 4 is overexpressed in human hepatocellular carcinoma
Sung, Young Kwan,Hwang, Sun Young,Park, Mi Kyung,Bae, Han Ik,Kim, Woo Ho,Kim, Jung-Chul,Kim, Moonkyu Wiley (Blackwell Publishing) 2003 Cancer Science Vol.94 No.5
<P>Fatty acid-CoA ligase 4 (FACL4) is a central enzyme controlling the unesterified arachidonic acid (AA) level in cells. It has been shown that FACL4 blocks apoptosis and promotes colon carcinogenesis by lowering the cellular level of unesterified AA. Consistent with this, FACL4 is upregulated in colon adenocarcinoma. The status of FACL4 in other tumors including hepatocellular carcinoma (HCC) is not known. Here, we report that FACL4 is overexpressed in human HCC compared with adjacent normal liver tissues. FACL4 mRNA and protein were overexpressed in 5 out of 12 (41.7%) and 3 out of 8 (37.5%) cases of HCC, respectively. Immunohistochemical staining showed strong fine granular intracytoplasmic staining in tumor cells, whereas we observed occasional weak staining in normal liver tissues surrounding the tumors. We found that 14 out of 37 (37.8%) HCC expressed moderate to strong FACL4 immunostaining. Both normal adult and fetal liver tissues showed very weak to no detectable staining, whereas 3 out of 10 (30%) cirrhotic livers expressed weak staining. In addition, we found that 4 out of 8 (50%) human hepatoma cell lines expressed high levels of FACL4 by northern blot analysis. Our results show that FACL4 is a new molecular marker for HCC and suggest that the FACL4 pathway may be involved in liver carcinogenesis.</P>
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