Development and Validation of Reconfigurable Autonomous Mobile Manipulator for Flexible Manufacturing Process

Okjoon Lee,Doyoung Kim,Yujin Kim,Wonseok Kim,Seungwon Lee,Dong Yeop Kim,Young-Ouk Kim,Keunhwan Kim 제어로봇시스템학회 2023 제어로봇시스템학회 국제학술대회 논문집 Vol.2023 No.10

치은 섬유아세포와 타액선 세포주에서 유지놀 처리에 따른 고사에 관한 연구

OkJoon Kim,HyangSuk Park,HongRan Choi 대한구강악안면병리학회 2004 대한구강악안면병리학회지 Vol.28 No.1

Eugenol (4-allyl-2-methoxyphenol) is a phenol derivative and generally used in dental treatment. A few investigator reported that eugen이-induced C)πoto잉city by apopto디c pathway, but it is not yet well understood In the present study, to investigate the eugenol-induced cytoto잉city by apoptosis, we have examined the apoptotic molecules and pathway in primary human gingival fibroblast (HGF) and human salivary gland cells (HSG). To identify apoptotic cell death, 3-(4,5-dimethylthiazol-2-yl)-2 ,5-diphenyl tetrazolium bromide (MTT) reduction assay with or without N-acetylcysteine (NAC), and the morphological study by propidium iodide (pI) staining were screened. And to investigate the apoptotic pathway, reverse transcriptase-polymerase chain reaction (RT-PCR) for apoptotic molecules and caspase aαivity assay were performed. Both M1T reduction assay and an addition of NAC showed that eugenol act as a pro-oxidant led to cell death. With the morphological study, both cells showed apoptotic change by nuclear fragmentation and/or chromatin condensations. With the apoptotic machinery study, the Bax and Bcl-2 mRNA expression were not detected in HGF. But, for HSG, the increased expression of Bax with decreased of Bcl-2 was observed. And the expression of Apaf-l was not detected or nα significantly increased in HGF and HSG, respectively. With measure of caspase activity, there was no change of caspase activities in HGF. But, for HSG, there was decrease of caspase 9 activity and increased caspase 3 activity. We suggest eugenol-treated HGF underwent apoptosis independent of Bcl family and caspase. However, for eugenol-πeated HSG, apoptosis occurred via Bcl famiIy and caspase pathway.

Immunohistochemical Study of Nitric Oxide Synthase in Pleomorphic Adenoma of the Salivary Glands

김옥준(Okjoon Kim),김도균(Dogyun Kim),정지연(Ji Yeun Jeong),김현진(Hyun Jin Kim),김원재(Won Jae Kim),최홍란(Hongran Choi),김선헌(Sunhun Kim) 대한해부학회 2003 Anatomy & Cell Biology Vol.36 No.2

산화질소는 신생혈관생성, 암종의 전이등 종양에 영향을 미치는 것으로 알려져 있으나, 머리 및 목에서 발생하는 종양 에 대한 산화질소 활성도에 관한 연구는 거의 없다. 본 연구는 침샘에서 발생하는 양성 종양 중 가장 빈번한 다형성 선종 및 인접 정상조직에서 eNOS (산화질소합성효소) 및 iNOS의 발현도를 알아보기 위해 면역조직화학검사를 시행하였다. 면역조직화학검사 결과 다형성 선종에서 인접 정상조직보다 높은 NOS의 발현을 보였는데, 이는 산화질소합성효소의 증가가 종양 생성 및 진행과 관련성이 있음을 시사한다. 또한, NOS 발현은 간엽성 유래 구성요소 보다는 상피성 유래 구성요소에서 더 높게 발현되었다. 대체로 다형성 선종에서는 iNOS의 발현이 eNOS보다 높게 나타났다. 다형성 선종에 인접한 정상조직에서 iNOS의 발현은 간엽성이 우세한 것보다 상피성이 우세한 다형성 선종에서 더 높게 발현되어 eNOS보다는 iNOS 가 종양의 진행에 더 관여할 것으로 추측된다. 결론적으로 산화질소는 종양의 초기성장과 진행에 있어 중요한 인자이며, 앞으로 종양 성장에 중요한 인자인 신생혈관생성에 관련한 인자와 함께 더 많은 연구가 필요할 것으로 사료된다. Recent studies have suggested that nitric oxide (NO) exerts various effects on aspects of tumor biology, including angiogenesis and metastasis. There have been, however, scanty reports on nitric oxide synthase (NOS) response for tumors of the head and neck. This study was carried out to assess the distribution of both endothelial NOS (eNOS) and inducible NOS (iNOS) in normal salivary gland tissue and in pleomorphic adenoma by using immunohistochemistry. In the present study, eNOS and iNOS were higher expressed in pleomorphic adenoma than adjacent normal salivary gland tissue, suggesting that up-regulation of this enzyme is associated with tumor progression. Additionally, eNOS and iNOS expression were higher in epithelial components than in mesenchymal components. Overall, iNOS expression was higher than eNOS expression in pleomorphic adenoma. In normal tissues adjacent to pleomorphic adenoma, iNOS expression was higher in the mesenchymal type than in the epithelial type of pleomorphic adenoma. It is suggested that NO may play a role in the tumorgenesis and propagation of pleomorphic adenoma.

Feruloylserotonin inhibits hydrogen peroxide-induced melanogenesis and apoptosis in B16F10 and SK-Mel-2 melanoma cells

Cho, Hyejoung,Kim, Okjoon,Lee, Younghee,Kang, Li-Jung,Nguyen, Cam Ngoc,Ishihara, Atsushi,Kim, Hye-Eun Elsevier 2017 Biochemical and biophysical research communication Vol. No.

<P><B>Abstract</B></P> <P>Feruloylserotonin (FS) is a major bioactive component of safflower seeds, with documented strong antibacterial, anti-inflammatory, and free radical scavenging activities. Reactive oxygen species (ROS) can strongly induce melanogenesis and cell apoptosis. The present study aimed to investigate the ability of FS in preventing hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>)-induced melanogenesis and cell apoptosis. Melanogenesis and apoptotic cell death were induced by transient exposure to H<SUB>2</SUB>O<SUB>2</SUB> in B16F10 and SK-Mel-2 melanoma cells. FS significantly inhibited melanogenesis and cell death in both cell lines. FS inhibited H<SUB>2</SUB>O<SUB>2</SUB>-induced melanin production by down-regulating CREB/MITF/TYR signaling via inhibited intracellular cAMP accumulation. Additionally, FS induced extracellular regulated kinase activation, which led to the degradation of MITF and consequently decreased TYR expression and melanin production in H<SUB>2</SUB>O<SUB>2</SUB>-stimulated cells. Furthermore, FS inhibited H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptotic cell death by maintaining mitochondrial membrane potential. Therefore, FS might have potential use for cosmetic whitening and as a therapeutic agent for hyperpigmentation disorder.</P> <P><B>Highlights</B></P> <P> <UL> <LI> FS inhibited H<SUB>2</SUB>O<SUB>2</SUB>-induced melanogenesis by down-regulating the cAMP/CREB/MITF/TYR signaling. </LI> <LI> FS also regulated H<SUB>2</SUB>O<SUB>2</SUB>-induced melanogenesis via activation of p-ERK, which led to the degradation of MITF. </LI> <LI> FS protected cells from H<SUB>2</SUB>O<SUB>2</SUB>-induced apoptosis by maintaining mitochondrial membrane potential. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

Ultraviolet-C-Induced Apoptosis Protected by 635-nm Laser Irradiation in Human Gingival Fibroblasts

Lim, Wonbong,Ko, Mikyung,Lee, Sungga,Kim, Inae,Jung, Mina,Kim, Okjoon,Cho, Seonghoun,Yang, Kyuho,Choi, Namki,Kim, Sunmi,Choi, Hongran Mary Ann Liebert 2008 Photomedicine and laser surgery Vol.26 No.3

<P>OBJECTIVE: The purpose of this study was to examine the protection afforded by 635-nm irradiation against ultraviolet (UV)-C-induced apoptosis in primary human gingival fibroblasts (hGFs). BACKGROUND DATA: UV irradiation is known to cause photoaging and cellular apoptosis of skin cells and is considered to be one of the leading causes of skin carcinogenesis. MATERIALS AND METHODS: To induce apoptosis, UV-C (100 mJ/cm2) was used to irradiate hGFs. To protect them from apoptosis, pretreatment with 635-nm irradiation was performed for 1 h immediately after cell plating 36 or 48 h before UV-C irradiation. The light source used for irradiation was a continuous-wave 635-nm LED laser emitting at 1 mW/cm2. Experimental samples were selected 24 h after UV-C irradiation. To measure the numbers of apoptotic cells, MTT assay and flow cytometric analyses were performed. For histomorphologic findings, Diff-Quick staining was carried out. Also, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were measured. RESULTS: In the present study, the number of apoptotic cells declined in the cells that were pretreated with 635-nm light irradiation in a time-dependent manner. In addition, the activities and mRNA expression of caspase-3, caspase-8, and caspase-9 were significantly recovered by pretreatment with 635-nm irradiation. CONCLUSION: These results suggest that 635-nm visible light irradiation may be used as a protective tool to prevent UV-C-induced apoptosis.</P>

Red light-emitting diode irradiation regulates oxidative stress and inflammation through SPHK1/NF-κB activation in human keratinocytes

Sun, Qiaochu,Kim, Hye-Eun,Cho, Hyejoung,Shi, Shuhan,Kim, Byungkuk,Kim, Okjoon Elsevier 2018 Journal of photochemistry and photobiology Biology Vol.186 No.-

<P><B>Abstract</B></P> <P>Oxidative stress, in which the amount of oxidants exceeds the capacity of antioxidant defense system, is a well-accepted pathogenesis of several human diseases. Light-emitting diode irradiation (LEDI) is an efficient strategy to counteract this condition. The biological effect of phototherapy, using visible light, has attracted recent attention especially in dermatological practice. However, little is known about the molecular mechanism of the anti-oxidant and anti-inflammatory effects of red light irradiation. We evaluated these effects of LEDI in HaCaT human keratinocyte cells under phorbol-12-myristate-13-acetate (PMA) induced reactive oxygen species (ROS). Microarray analysis revealed changes in 309 genes after LEDI. LEDI at 625 nm produced ROS scavenging and anti-inflammatory effects. One of the most important genes identified by microarray analysis was sphingosine kinase-1 (SPHK1), which is a key molecule in sphingolipid metabolism. SPHK1 knock-down drastically reduced ROS scavenging efficiency as well as expression levels of inflammation-related proteins in PMA-treated HaCaT cells. These results not only indicate the potential for the clinical application of 625-nm LEDI in treating skin disorders via ROS and/or inflammation, but also suggest SPHK1 as a potential therapeutic target in phototherapy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> LEDI at 625 nm produced ROS scavenging and anti-inflammation. </LI> <LI> Sphingosine kinase-1 (SPHK1) was identified by microarray analysis in the experimental conditions. </LI> <LI> LEDI 625 nm has the potential for treating skin disorder via ROS and/or inflammation through SPHK1/NF-κB pathway. </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>

광 감응성 물질의 세포내 위치에 따른 Photodynamic therapy(PDT) 의 세포사멸 경로에 관한 연구

WonBong Lim,SungGa Lee,InAe Kim,MinA Jung,OkJoon Kim,HongRan Choi 대한구강악안면병리학회 2007 대한구강악안면병리학회지 Vol.31 No.5

Photodynamic therapy(PDT) 는 특정 광 감응 물질 에 광 조사를 수행하여 세 포내애서 활성 산소종(ROS) 의 증가를 통한 암세 포의 사띨을 유도하는 방법이다 광 감응 물질은 암세 포에 선택 적으로 흡수되어 특정 파장의 빛을 홉수하여 다량의 ROS를 발생하여 암세 포의 사멸을 유도한다, 그러나 PDT 수행 시 ROS의 세 포내 작용에 따른 사띨 기전 이 영확히 알려지 지 않았고, 비 선 택 성으로 인한 정 상 세포애서의 피해 도 유발될 수 있다고 보고되었다 본 연 구애서 는 굉 감웅제인 He ma to por p h y rin을 이 용하여 구깅암 세포주인 He p2에서 광조사를 통한 세포 사멸 에 관한 연 구를 수행하였다 Confocal mi crosco py를 통한 분석에서 Hemato po r phyrin은 홉수 시 간에 따라 세포막에서 세 포질 핵 으로의 위치함을 관찰 할 수 있었고. 전기 영 동에 따른 DNA 분절 분석에서 24 시간이상 홉수된 상태 에서 ladder 패턴을 보임으로써 세 포 자띨사에 이 르는 만웅을 보였다 DCF - DA에 의힌 세 포내 ROS 분석 을 수행힌 결과 Hema to po rphyrin의 흡수 시간이 증가할수록 세포 내부에서의 ROS 발생이 증가함을 획 인 할 수 있었 다 이와 같은 결과에 따르면 Hematoporphyrin을 이용한 PDT에서 h ematoporphy ri n의 홉수 시 간에 따라 세 포 자띨사가 유도되었고. 특히 Hematoporphyrin은 흡수 시 간이 증가하여 세 포 내 부까지 충분히 Hematoporphyri n 이 작용된 경우에 서 ‘ ROS 발생애 따른 미 토콘드리아 의존적 경 로를 통해 세 포 자멸사가 유도되 었음을 확인 할 수 있었다-

Treatment of mutant RANKL on RANKL-induced mice for osteoporosis

Bora KIM,Dahye KWON,Serim KIM,Sangil LIM,Changju AN,Okjoon KIM,Wonbong LIM 한국생물공학회 2018 한국생물공학회 학술대회 Vol.2018 No.10

Cell proliferation and migration mechanism of caffeoylserotonin and serotonin via serotonin 2B receptor in human keratinocyte HaCaT cells

( Hye-eun Kim ),( Hyejoung Cho ),( Atsushi Ishihara ),( Byungkuk Kim ),( Okjoon Kim ) 생화학분자생물학회(구 한국생화학분자생물학회) 2018 BMB Reports Vol.51 No.4

Caffeoylserotonin (CaS), one derivative of serotonin (5-HT), is a secondary metabolite produced in pepper fruits with strong antioxidant activities. In this study, we investigated the effect of CaS on proliferation and migration of human keratinocyte HaCaT cells compared to that of 5-HT. CaS enhanced keratinocyte proliferation even under serum deficient condition. This effect of CaS was mediated by serotonin 2B receptor (5-HT2BR) related to the cell proliferation effect of 5-HT. We also confirmed that both CaS and 5-HT induced G1 progression via 5-HT2BR/ERK pathway in HaCaT cells. However, Akt pathway was additionally involved in upregulated expression levels of cyclin D1 and cyclin E induced by CaS by activating 5-HT2BR. Moreover, CaS and 5-HT induced cell migration in HaCaT cells via 5-HT2BR. However, 5-HT regulated cell migration only through ERK/AP-1/MMP9 pathway while additional Akt/NF-κB/MMP9 pathway was involved in the cell migration effect of CaS. These results suggest that CaS can enhance keratinocyte proliferation and migration. It might have potential as a reagent beneficial for wound closing and cell regeneration. [BMB Reports 2018; 51(4): 188-193]

Development of Novel Photosensitizer Using the <i> Buddleja officinalis</i> Extract for Head and Neck Cancer

Cho, Hyejoung,Zheng, Hui,Sun, Qiaochu,Shi, Shuhan,He, YuZhu,Ahn, Kyuhyeon,Kim, Byunggook,Kim, Hye-Eun,Kim, Okjoon Hindawi 2018 Evidence-based Complementary and Alternative Medic Vol.2018 No.-

<P>Photodynamic therapy (PDT) is generally safer and less invasive than conventional strategies for head and neck cancer treatment. However, currently available photosensitizers have low selectivity for tumor cells, and the burden and side effects are so great that research is needed to develop safe photosensitizers. In this study, it was confirmed that the<I> Buddleja officinalis</I> (BO) extract, used in the treatment of inflammation and vascular diseases, shows fluorescence when activated by LED light, and, based on this, we aimed to develop a new photosensitive agent suitable for PDT. MTT, Diff-Quick® staining, and DCF-DA were performed to measure the effects of treating head and neck cancer cells with BO extract and 625 nm LED light (BO-PDT). Cell cycle, TUNEL, and western blot assays, as well as acridine orange staining, were performed to explore the mechanism of BO-PDT-induced cell death. We found that when the BO extract was irradiated with 625 nm LED light, it showed sufficient fluorescence and stronger intracellular toxicity and ROS effect than the currently commercially available hematoporphyrin. BO-PDT resulted in a decrease of mTOR activity that was correlated with an increase in the levels of ATG5, beclin-1, and LC3-II, which interfere with the formation of autophagosomes. In addition, BO-PDT induced the activation of PARP and led to an increase in the expression of proapoptotic protein Bax and a decrease in the expression of the antiapoptotic protein Bcl-2. Moreover, BO-PDT has been shown to induce the autophagy pathway 4 h after treatment, while apoptosis was induced 16 h after treatment. Finally, we confirmed that BO-PDT caused cell death of head and neck cancer cells via the intrinsic pathway. Therefore, we suggest that BO extract can be used as a new photosensitizer in PDT of head and neck cancer.</P>