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표정인식을 위한 PCA와 템플릿 정합을 사용한 얼굴 요소 추출
우효정, 이슬기, 김동우, 류성필, 안재형 충북대학교 산업과학기술연구소 2013 산업과학기술연구 논문집 Vol.27 No.2
This paper proposed an extracting algorithm of human facial components for the recognition of facial expressions. First face image is acquired using the Haar-like feature mask from an input image. The face image is divided into two images. One is the upper image including eye and eyebrow. The other is the lower image including mouth and jaw. The extraction of facial components, such as eye and mouth, begins getting eye image and mouth image. Then eigenfaces are produced by the PCA training process with learning images. An eigeneye and an eigenmouth are produced from eigenfaces. Result eye image is obtained by template matching the upper image with the eigeneye, and the mouth image is obtained by template matching the lower image with the eigenmouth. The simulation results show that the proposed method has superior extraction ratio than previous method.
( Dam Kim ),( Soo-kyung Cho ),( Seoung Wan Nam ),( Hyuk Hee Kwon ),( Sun-young Jung ),( Chan Hong Jeon ),( Seul Gi Im ),( Dalho Kim ),( Eun Jin Jang ),( Yoon-kyoung Sung ) 대한류마티스학회 2017 대한류마티스학회지 Vol.24 No.5
Objective. To estimate the cardiovascular (CV) and gastrointestinal (GI) risks of etoricoxib in the treatment of osteoarthritis (OA) compared to a placebo and other non-steroidal anti-inflammatory drugs (NSAIDs). Methods. A systematic review of randomized, controlled trials (RCTs) of etoricoxib were performed. Bayesian network meta-analysis was used over a duration of 12 weeks. The incidence of CV and GI events for a duration ≥26 weeks were also tabulated and presented using descriptive statistics. Results. From this search, 10 studies were identified. Of these, 6 and 5 RCTs that measured the CV and GI events at 12 weeks were included in meta-analysis. They showed that etoricoxib did not increase the CV events compared to the placebo or NSAIDs during the 12 week period (odds ratio [OR]=0.59 compared to celecoxib, OR=0.89 with ibuprofen, OR=0.70 with placebo, and OR=2.16 with naproxen). The risk of GI events was comparable to that of most comparators, with the exception of naproxen, which had a significantly lower risk of GI events (OR=0.18) during the 12 week period. For a duration ≥26 weeks, the incidence of CV and GI events with etoricoxib increased with increasing duration. Conclusion. Etoricoxib is an alternative short-term treatment option for OA, showing comparable CV and GI complications to other NSAIDs. Nevertheless, further studies will be needed to elucidate the long-term safety of etoricoxib in the treatment of OA. (J Rheum Dis 2017;24:293-302)
Obesity induced by high fat diet in Rhomboid family member 2 (Rhbdf2) KO mice
Sung-Jun Kim(Sung-Jun Kim),Seul Gi Park(Seul Gi Park),Young-Sub Byun(Young-Sub Byun),Eun-Kyoung Kim(Eun-Kyoung Kim),Sang-Mi Cho(Sang-Mi Cho),Harim Kim(Harim Kim),Young-Suk Won(Young-Suk Won),Hyoung-Ch 한국예방수의학회 2017 한국예방수의학회 학술대회자료집 Vol.2017 No.-
Kim Dabin,Kim Min Hye,Park Seul Gi,Choi Sujin,Lee Chan Jae,Jung Young Hwa,Choi Chang Won,Shin Myoung-Jin,Song Kyoung-Ho,Kim Eu Suk,Park Jeong Su,Kim Hong Bin,Lee Hyunju 대한소아감염학회 2023 Pediatric Infection and Vaccine Vol.30 No.1
A case of persistent Ralstonia mannitolilytica bacteremia in the neonatal intensive care unit prompted source investigation due to its rarity. After an extensive investigation, a contaminated ultrasonic nebulizer was identified as the source, and the infection was controlled by removing the source. This study emphasizes the importance of further investigations, even in single cases of rare pathogens.
Seul Gi Park,Eun-kyoung Kim,Hyoung-Chin Kim,Won-Kee Yoon,Ki-Hoan Nam,Sang-Yoon Nam 한국실험동물학회 2021 한국실험동물학회 학술발표대회 논문집 Vol.2021 No.7
Asb2, ankyrin repeat and SOCS box protein 2 form an E3 ubiquitin ligase complex. Asb2 ubiquitin ligase activity drives the degradation of filamins, which have essential functions in humans [1, 2]. The placenta is a temporary organ that is formed during pregnancy, and normal placentation is important for survival and growth of the fetus [3]. Recent studies have shown that approximately 25-30% of knockout (KO) mice have non-viable offspring, and 68% of knockout lines exhibit placental dysmorphologies [4]. There are very few studies on Asb2, with insufficient researches on its role in placental development. We generated Asb2 knockout mice and investigated Asb2 expression during organogenesis, and identified its role in early embryonic and placental development. The external morphology of KO embryos revealed abnormal phenotypes including growth retardation, peri-cardial effusion, pale color, and especially heart beat defect from E 9.5. Furthermore, Asb2 expression was observed in the heart from E 9.5, indicating that it is specifically expressed during early heart formation and defects, result in embryonic lethality. Histological analysis of E 10.5 KO mouse heart showed malformations such as failure of chamber formation, reduction in trabeculated myocardium length, absence of mesenchymal cells, and destruction of myocardial wall. Moreover, the histological observation of the placenta for Asb2-deficient mice showed abnormal phenotypes including small labyrinth and reduced vascular complexity, indicating that failure to establish mature circulatory pattern affects the embryonic development and associated with the early mortality. Collectively, our results demonstrate that Asb2 knockout mice have placental defects, and failure to form a normal cardiac septum, and thereby result in embryonic lethality in utero at around E 9.5. References [1] Babon, J.J., et al., The SOCS box domain of SOCS3: structure and interaction with the elonginBC-cullin5 ubiquitin ligase. J Mol Biol, 2008. 381(4): p. 928-40.[2] Heuze, M.L., et al., ASB2 is an Elongin BC-interacting protein that can assemble with Cullin 5 and Rbx1 to reconstitute an E3 ubiquitin ligase complex. J Biol Chem, 2005. 280(7): p. 5468-74.[3] Cross, J.C., D.G. Simmons, and E.D. Watson, Chorioallantoic morphogenesis and formation of the placental villous tree. Ann N Y Acad Sci, 2003. 995: p. 84-93.[4] Rossant, J. and J.C. Cross, Placental development: lessons from mouse mutants. Nat Rev Genet, 2001. 2(7): p. 538-48.
Kim, Myeong Seop,Ryu, HyungChul,Kang, Dong Wook,Cho, Seong-Hee,Seo, Sejin,Park, Young Soo,Kim, Mi-Yeon,Kwak, Eun Joo,Kim, Yong Soo,Bhondwe, Rahul S.,Kim, Ho Shin,Park, Seul-gi,Son, Karam,Choi, Sun,DeA American Chemical Society 2012 Journal of medicinal chemistry Vol.55 No.19
<P>A series of <I>N</I>-(2-amino-6-trifluoromethylpyridin-3-ylmethyl)-2-(3-fluoro-4-methylsulfonylaminophenyl)propanamides were designed combining previously identified pharmacophoric elements and evaluated as hTRPV1 antagonists. The SAR analysis indicated that specific hydrophobic interactions of the 2-amino substituents in the C-region of the ligand were critical for high hTRPV1 binding potency. In particular, compound <B>49</B><I><B>S</B></I> was an excellent TRPV1 antagonist (<I>K</I><SUB>i(CAP)</SUB> = 0.2 nM; IC<SUB>50(pH)</SUB> = 6.3 nM) and was thus approximately 100- and 20-fold more potent, respectively, than the parent compounds <B>2</B> and <B>3</B> for capsaicin antagonism. Furthermore, it demonstrated strong analgesic activity in the rat neuropathic model superior to <B>2</B> with almost no side effects. Compound <B>49</B><I><B>S</B></I> antagonized capsaicin induced hypothermia in mice but showed TRPV1-related hyperthermia. The basis for the high potency of <B>49</B><I><B>S</B></I> compared to <B>2</B> is suggested by docking analysis with our hTRPV1 homology model in which the 4-methylpiperidinyl group in the C-region of <B>49</B><I><B>S</B></I> made additional hydrophobic interactions with the hydrophobic region.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jmcmar/2012/jmcmar.2012.55.issue-19/jm300780p/production/images/medium/jm-2012-00780p_0014.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/jm300780p'>ACS Electronic Supporting Info</A></P>
Seul Gi Kim,Jin Young Sung,Jae-Ryong Kim,Hyoung Chul Choi 대한생리학회-대한약리학회 2020 The Korean Journal of Physiology & Pharmacology Vol.24 No.1
Aging is one of the risk factors for the development of cardiovascular diseases. During the progression of cellular senescence, cells enter a state of irreversible growth arrest and display resistance to apoptosis. As a flavonoid, quercetin induces apoptosis in various cells. Accordingly, we investigated the relationship between quercetin-induced apoptosis and the inhibition of cellular senescence, and determined the mechanism of oxidative stress-induced vascular smooth muscle cell (VSMC) senescence. In cultured VSMCs, hydrogen peroxide (H2O2) dose-dependently induced senescence, which was associated with increased numbers of senescenceassociated β-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Along with senescence, expression of the antiapoptotic protein Bcl-2 was observed to increase and the levels of proteins related to the apoptosis pathway were observed to decrease. Quercetin induced apoptosis through the activation of AMP-activated protein kinase. This action led to the alleviation of oxidative stress-induced VSMC senescence. Furthermore, the inhibition of AMPK activation with compound C and siRNA inhibited apoptosis and aggravated VSMC senescence by reversing p53-p21 and p16 pathways. These results suggest that senescent VSMCs are resistant to apoptosis and quercetin-induced apoptosis attenuated the oxidative stress-induced senescence through activation of AMPK. Therefore, induction of apoptosis by polyphenols such as quercetin may be worthy of attention for its anti-aging effects.
Kim, Kwang-Youn,Park, Kwang-Il,Lee, Seul Gi,Baek, Su Youn,Lee, Eun Hye,Kim, Sang Chan,Kim, Sang-Hun,Park, Sul-Gi,Yu, Sun-Nyoung,Oh, Tae Woo,Kim, Joung-Hee,Kim, Keuk-Jun,Ahn, Soon-Cheol,Kim, Young Woo Elsevier 2018 Chemico-biological interactions Vol.294 No.-
<P><B>Abstract</B></P> <P>Deoxypodophyllotoxin (DPT) is a naturally occurring flavolignan in <I>Anthriscus sylvestris</I> known as cow parsley or wild chervil, and has been reported to have inhibitory effects against several pathological processes including cancer, inflammation and infection. Here, we report the effects of DPT in the fatty liver induced by high fat diet <I>in vivo</I> as well as its regulatory mechanism related with the transcription factor for lipogenic genes such as sterol regulatory element binding protein-1c (SREBP-1c) <I>in vitro</I>. C57BL/6 mice were fed high fat diet for 10 weeks and also orally administrated with DPT for additional 4 weeks. 5 and 10 mg/kg of DPT decreased lipid accumulation in the liver induced by high fat diet, as indicated by histological parameters such as Oil Red O staining and hematoxylin & eosin as well as the contents of hepatic triglyceride and cholesterol. In hepatocytes, DPT inhibited the liver X receptor α-mediated SREBP-1c induction and expression of the lipogenic genes, including fatty acid synthase, acetyl-CoA carboxylase and stearoyl-CoA desaturase-1. Moreover, DPT induced AMP-activated protein kinase (AMPK) activation, which has been known to inhibit the expression of SREBP-1c in hepatocyte. Also this compound restored the dysregulation of AMPK and SREBP-1c induced by high fat diet in mice. In conclusion, we demonstrated that DPT significantly inhibited fatty liver by adjusting lipid metabolism coordinated with AMPK activation and SREBP-1c inhibition.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Deoxypodophyllotoxin (DPT), a chemopreventive flavolignan, inhibited diet-induced fatty liver. </LI> <LI> DPT inhibited the LXR-α-mediated sterol regulatory element binding protein (SREBP)-1c. </LI> <LI> DPT blocked the expression of <I>de novo</I> lipogenic genes including FAS and ACC. </LI> <LI> DPT activated AMPK related with SREBP-1c inhibition. </LI> <LI> DPT might be a pharmaceutical candidate for hepatic steatosis. </LI> </UL> </P>
Kim, Kwang-Youn,Lee, Seul-Gi,Baek, Su Youn,Lee, Eun Hye,Jang, Eun Jeong,Lee, Ju-Hee,Ahn, Soon-Cheol,Chang, Jae-Hoon,Oh, Tae Woo,Kim, Sang-Hun,Ma, Jin-Yeul,Kim, Sang Chan,Park, Kwang-Il,Kim, Young Woo Elsevier 2018 Toxicology and applied pharmacology Vol.360 No.-
<P><B>Abstract</B></P> <P>Salinomycin, a monocarboxylic ionophore in <I>Streptomyces albus</I>, has been studied as an anti-cancer agent. However, we wondered whether salinomycin has another effect such as an anti-oxidant and hepatic protectant, because some chemical drugs treating human diseases were sometimes related with their toxic effects. Therefore, this study was conducted to examine the effects of salinomycin against oxidative stress and mitochondrial impairment in vivo and in vitro as well as the cellular mechanisms of action. In hepatocyte, salinomycin inhibited arachidonic acid (AA) + iron-induced apoptosis, mitochondrial dysfunction and ROS production. As a molecular mechanism, salinomycin induced autophagy through AMP-activated protein kinase (AMPK) activation, as assessed by the accumulation of acidic vesicle organelles, p62 and LC3-II. Moreover, these protective effects were blocked by AMPK inhibition, which indicates the importance of AMPK in the process of salinomycin's effects. In mice, oral administration of salinomycin protected against carbon tetrachloride (CCl<SUB>4</SUB>)-induced oxidative stress and liver injury, and also activated AMPK as well as autophagy-related proteins in the liver. Collectively, salinomycin had the ability to protect hepatocytes against AA+iron-induced reactive oxygen species production and mitochondrial dysfunction, as well as CCl<SUB>4</SUB>-induced liver injury. Although this beneficial effect was demonstrated under severe oxidative stress, this study showed that salinomycin protected the liver against the oxidative stress and liver damage through AMPK and autophagy, and suggest that salinomycin has a possibility to treat a broad range of diseases.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>