아끼시나무의 신용도 개발 : 온돌용 바닥재 제조 Manufacture of Floor for Ondol

노정관,윤석규 진주산업대학교 1999 산업과학기술연구소보 Vol.- No.6

아까시나무재의 色相과 强度的 性能등의 材質을 고려한 새로운 用途로서 2종류의 온돌용마루판 제조와 그 성능늘 검토하였다. 1.合成樹脂 複合 아까시나무 溫突用 마루板 0.5㎜ 아까시나무 單板과 ABS(아크릴로니트릴-부타디엔-스틸렌)樹脂를 이용하여 10x10㎝의 아까시나무 溫突用 마루板을 射出成形하여 製造하였다. 본 제품의 熱傳達速度는 市販의 溫突用 마루板 에비해 비교적 양호하였으며, 熱變形溫度는 160℃로 온돌 위에 시공하여 이용하여도 열에 의한 문제는 없을 것으로 생각된다. 또한, 휨강도도 아까시나무 素材와 거의 유사하였으며, 市販의 온돌용 마루판에 비해서는 우수하였다. 合成樹脂와 아까시나무 單板間의 耐水接着性能은 1시간 끓임과 60℃, 20時間乾燥 후에도 剝籬되지 않았다. 2.폐비닐 複合 아까시나무 溫突用 마루板 폐비닐, 탈크 및 목분을 組合하여 製造한 시트상의 基材에 0.5㎜ 아까시나무 單板을 積層接着하여 製造하였다.두께가 3.2㎜로 기존의 제품에 비해 얇기 때문에 熱傳達 性能이 우수하고, 再生樹脂板體와 아까시나무 單板間의 耐水 接着性能 및 耐熱性도 비교적 良好하였다. This research was endeavored to manufacture two kinds of Ondol floor made of Black Locust with consideration of color and strength, and the bonding properties were evaluated. 1.Composite Ondol floor with locust veneer and synthetic resin The Ondol floor (10 by 10㎝) was manufactured by injection moulding with locust veneer (thickness 0.5㎜) and ABS (acrylonitry-butadiene-styrene) resin. The heat transfer rate and bending strength of manufactured Ondol floor were comparatively higher than those of current commercial products, and the bending strength was even similar with locust lumber, In aspect of the water resistance(wet bonding property) between synthetic resin and locust veneer, the delamination was not occurred after 20 hours drying at 60℃ with 1 hour boiling. 2.Composite Ondol floor with locust veneer and recycled vinyl The Ondol floor was manufactured by laminating locust veneer (thickness 0.5㎜) with base plate on sheet containing recycled vinyl, talc and sawdust. Compared with current commercial products, the heat transfer property was superior due to slim thickness (3.2㎜). In addition, the heat resistance and water resistance between recycled resin plate and locust veneer were also suitable.

아까시나무의 신용도 개발 : 이용 현황과 집성 마루판 제조 Tendency of Utilization and Manufacture of Laminated Floor

노정관,윤석규 진주산업대학교 2000 산업과학기술연구소보 Vol.- No.7

This research was endeavored to manufacture two kinds of laminated floor made of Black Locust with consideration of color and strength, and to evaluate the bonding properties of Locust lamina bonded with various ambient setting resin adhesives. 1. Bonding properties of Black locust The superior bonding strengths of ambient setting resin uses in Black locust lamina were obtained in all resin used in this research, but wood failures were not cleared the KS in PVAc, Phenol·resorcinol and Oilic urethane resin. 2. Manufacture of Laminated floors Two kinds of laminated floor were manufactured by laminating with Black locust lamina. The laminated floor(900×80×15mm) was made of Locust lamina bonding with Urea, Water based polymer-isocyanate and Phenol·resorcinol resin adhesives. The other one was tile type laminated floor(90×90×15mm) which moulded to contain two tongues and two grooves.

한의진단명과 진단요건의 표준화 연구 III : 3차년도 연구결과 보고

최선미,양기상,최승훈,박경모,박종현,심범상,김성우,노석선,이인선,정진홍,이진용,김달래,임형호,김윤범,박성식,송태원,김종우,이승기,최윤정,신순식 한국한의학연구원 1997 한국한의학연구원논문집 Vol.3 No.1

The diagnostic requirements were suggested and explained regarding the systems of differentiation of symptoms and signs in the third year study of standardization and unification of the terms and conditions used for diagnosis in oriental medicine. The systems were as follows : - analyzing and differentiating of epidemic febrile disease - analyzing and differentiating in accordance with the Sasang constitution medicine based on four-type recognition - differentiation of disease according to pathological changes of Chong and Ren channels - standards for diagnosis of women's disease - standards for diagnosis of children's disease - standards for diagnosis of motor and sensor disturbance (-muscle. born, joint, etc.) - standards for diagnosis of neuropsychiatric disease - standards for diagnosis of five sense organ disease - standards for diagnosis of external disease The indivisual diagnosis pattern was arranged by the diagnostic requirements in the following order : another name, notion of diagnosis pattern, index of differentiation of symptoms and signs, the main point of diagnosis, analysis of diagnosis pattern, discrimination of diagnosis pattern, prognosis, a way of curing a disease, prescription, herbs in common use, disease appearing the diagnosis pattern, documents. The standards for diagnosis of each disease was arranged by the diagnostic requirements in the following order : another name, notion of disease, the main point of diagnosis, analyzing and differentiating of disease, analysis of disease, discrimination of disease, prognosis, a way of curing and prescription of disease, disease in western medicine appearing the disease in oriental medicine, documents.

Neuroprotective Effects of Ginsenoside Rg₃ against 24-OH-cholesterol-induced Cytotoxicity in Cortical Neurons

Yoon Seok Roh,Hyoung Bae Kim,Chang-Won Kang,Bum Seok Kim,Seung-Yeol Nah,Jong-Hoon Kim 고려인삼학회 2010 Journal of Ginseng Research Vol.34 No.3

Ginsenoside Rg₃ (Rg₃), one of the active ingredients in Panax ginseng, attenuates NMDA receptor-mediated currents in vitro and antagonizes NMDA receptors through a glycine modulatory site in rat cultured hippocampal neurons. In the present study, we examined the neuroprotective effects of Rg₃ on 24-hydroxycholesterol (24-OH-chol)-induced cytotoxicity in vitro. The results showed that Rg₃ treatment significantly and dose-dependently inhibited 24-OH-chol-induced cell death in rat cultured cort ical neurons, with an IC?? value of 28.7 ± 7.5 ㎛. Furthermore, the Rg₃ treatment not only significantly reduced DNA damage, but also dose-dependently attenuated 24-OH-chol-induced caspase-3 activity. To study the mechanisms underlying the in vitro neuroprotective effects of Rg₃ against 25-OH-chol-induced cytotoxicity, we also examined the effect of Rg₃ on intracellular Ca²? elevations in cultured neurons and found that Rg₃ treatment dose-dependently inhibited increases in intracellular Ca²?, with an IC?? value of 40.37 ± 12.88 ㎛. Additionally, Rg₃ treatment dose-dependently inhibited apoptosis with an IC?? of 47.3 ± 14.2 ㎛. Finally, after confirming the protective effect of Rg₃ using a terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay, we found that Rg₃ is an active component in ginseng-mediated neuroprotection. These results collectively indicate that Rg₃-induced neuroprotection against 24-OH-chol in rat cortical neurons might be achieved via inhibition of a 24-OH-chol-mediated Ca²? channel. This is the first report to employ cortical neurons to study the neuroprotective effects of Rg₃ against 24-OH-chol. In conclusion, Rg₃ was effective for protecting cells against 24-OH-chol-induced cytotoxicity in rat cortical neurons. This protective ability makes Rg₃ a promising agent in pathologies implicating neurodegeneration such as apoptosis or neuronal cell death.

Lactobacillus Aggravate Bile Duct Ligation-Induced Liver Inflammation and Fibrosis in Mice

Yoon Seok Roh,Ara Cho,Youn-Soo Cha,Suk-Heung Oh,Chae Woong Lim,Bumseok Kim 한국독성학회 2018 Toxicological Research Vol.34 No.3

Lactobacillus (LAB) have been reported to exert both harmful and beneficial effects on human and animal health. Recently, it has been reported that dysbiosis and bacterial translocation contribute to liver fibrosis. However, the role of Gram-positive LAB in the situation of chronic liver diseases has not been yet elucidated. Liver injury was induced by bile duct ligation (BDL) in LAB or control-administered mice. Liver fibrosis was enhanced in LABadministered mice compared with control-treated mice as demonstrated by quantification of Sirius-red positive area, hydroxyproline contents and fibrosis-related genes (Col1α1, Acta2, Timp1, Tgfb1). Moreover, LAB-administered mice were more susceptible to BDL-induced liver injury as shown by increased ALT and AST level of LAB group compared with control group at 5 days post BDL. Consistent with serum level, inflammatory cytokines (TNF-α, IL-6 and IL-1β) were also significantly increased in LAB-treated mice. Of note, LAB-treated liver showed increased lipoteichoic acid (LTA) expression compared with control-treated liver, indicating that LABderived LTA may translocate from intestine to liver via portal vein. Indeed, responsible receptor or inflammatory factor (PAFR and iNOS) for LTA were upregulated in LAB-administered group. The present findings demonstrate that administration of LAB increases LTA translocation to liver and induces profibrogenic inflammatory milieu, leading to aggravation of liver fibrosis. The current study provides new cautious information of LAB for liver fibrosis patients to prevent the detrimental effect of LAB supplements.

Chemokines and Chemokine Receptors in the Development of NAFLD

Roh, Yoon-Seok,Seki, Ekihiro Kluwer Academic Publishers 2018 Advances in experimental medicine and biology Vol.1061 No.-

Neuroprotective Effects of Ginsenoside Rg₃ against 24-OH-cholesterol-induced Cytotoxicity in Cortical Neurons

Roh, Yoon-Seok,Kim, Hyoung-Bae,Kang, Chang-Won,Kim, Bum-Seok,Nah, Seung-Yeol,Kim, Jong-Hoon The Korean Society of Ginseng 2010 Journal of Ginseng Research Vol.34 No.3

Ginsenoside $Rg_3$ ($Rg_3$), one of the active ingredients in Panax ginseng, attenuates NMDA receptor-mediated currents in vitro and antagonizes NMDA receptors through a glycine modulatory site in rat cultured hippocampal neurons. In the present study, we examined the neuroprotective effects of $Rg_3$ on 24-hydroxycholesterol (24-OH-chol)-induced cytotoxicity in vitro. The results showed that $Rg_3$ treatment significantly and dose-dependently inhibited 24-OH-chol-induced cell death in rat cultured cortical neurons, with an $IC_{50}$ value of $28.7{\pm}7.5\;{\mu}m$. Furthermore, the $Rg_3$ treatment not only significantly reduced DNA damage, but also dose-dependently attenuated 24-OH-chol-induced caspase-3 activity. To study the mechanisms underlying the in vitro neuroprotective effects of $Rg_3$ against 25-OH-chol-induced cytotoxicity, we also examined the effect of $Rg_3$ on intracellular $Ca^{2+}$ elevations in cultured neurons and found that $Rg_3$ treatment dose-dependently inhibited increases in intracellular $Ca^{2+}$, with an $IC_{50}$ value of $40.37{\pm}12.88\;{\mu}m$. Additionally, $Rg_3$ treatment dose-dependently inhibited apoptosis with an $IC_{50}$ of $47.3{\pm}14.2\;{\mu}m$. Finally, after confirming the protective effect of $Rg_3$ using a terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay, we found that $Rg_3$ is an active component in ginseng-mediated neuroprotection. These results collectively indicate that $Rg_3$-induced neuroprotection against 24-OH-chol in rat cortical neurons might be achieved via inhibition of a 24-OH-chol-mediated $Ca^{2+}$ channel. This is the first report to employ cortical neurons to study the neuroprotective effects of $Rg_3$ against 24-OH-chol. In conclusion, $Rg_3$ was effective for protecting cells against 24-OH-chol-induced cytotoxicity in rat cortical neurons. This protective ability makes $Rg_3$ a promising agent in pathologies implicating neurodegeneration such as apoptosis or neuronal cell death.

Toll-Like Receptor-7 Signaling Promotes Nonalcoholic Steatohepatitis by Inhibiting Regulatory T Cells in Mice

Roh, Yoon Seok,Kim, Jong Won,Park, Surim,Shon, Changho,Kim, Sokho,Eo, Seong Kug,Kwon, Jung Kee,Lim, Chae Woong,Kim, Bumseok Elsevier 2018 The American journal of pathology Vol.188 No.11

<P>Toll-like receptor 7 (TLR7) signaling regulates the production of type 1 interferons (IFNs) and proinflammatory cytokines, such as tumor necrosis factor (TNF)-α, implicated in the control of regulatory T (Treg) cell activity. However, the mechanistic interplay between TLR7 signaling and Treg cells in nonalcoholic steatohepatitis (NASH) has not been elucidated. Our aim was to clarify the role of TLR7 signaling in the pathogenesis of NASH. Steatohepatitis was induced in wild-type (WT), TLR7-deficient, IFN-α/β receptor 1–deficient, and Treg cell–depleted mice. TLR7-deficient and IFN-α/β receptor 1–deficient mice were more protective to steatohepatitis than WT mice. Of interest, both TNF-α and type 1 IFN promoted apoptosis of Treg cells involved in the prevention of NASH. Indeed, Treg cell–depleted mice had aggravated steatohepatitis compared with WT mice. Finally, treatment with immunoregulatory sequence 661, an antagonist of TLR7, efficiently ameliorated NASH <I>in vivo</I>. These results demonstrate that TLR7 signaling can induce TNF-α production in Kupffer cells and type I IFN production in dendritic cells. These cytokines subsequently induce hepatocyte death and inhibit Treg cells activities, leading to the progression of NASH. Thus, manipulating the TLR7-Treg cell axis might be used as a novel therapeutic strategy to treat NASH.</P>

Lactobacillus Aggravate Bile Duct Ligation-Induced Liver Inflammation and Fibrosis in Mice

Roh, Yoon Seok,Cho, Ara,Cha, Youn-Soo,Oh, Suk-Heung,Lim, Chae Woong,Kim, Bumseok Korean Society of ToxicologyKorea Environmental Mu 2018 Toxicological Research Vol.34 No.3

Lactobacillus (LAB) have been reported to exert both harmful and beneficial effects on human and animal health. Recently, it has been reported that dysbiosis and bacterial translocation contribute to liver fibrosis. However, the role of Gram-positive LAB in the situation of chronic liver diseases has not been yet elucidated. Liver injury was induced by bile duct ligation (BDL) in LAB or control-administered mice. Liver fibrosis was enhanced in LAB-administered mice compared with control-treated mice as demonstrated by quantification of Sirius-red positive area, hydroxyproline contents and fibrosis-related genes ($Col1{\alpha}1$, Acta2, Timp1, Tgfb1). Moreover, LAB-administered mice were more susceptible to BDL-induced liver injury as shown by increased ALT and AST level of LAB group compared with control group at 5 days post BDL. Consistent with serum level, inflammatory cytokines ($TNF-{\alpha}$, IL-6 and $IL-1{\beta}$) were also significantly increased in LAB-treated mice. Of note, LAB-treated liver showed increased lipoteichoic acid (LTA) expression compared with control-treated liver, indicating that LAB-derived LTA may translocate from intestine to liver via portal vein. Indeed, responsible receptor or inflammatory factor (PAFR and iNOS) for LTA were upregulated in LAB-administered group. The present findings demonstrate that administration of LAB increases LTA translocation to liver and induces profibrogenic inflammatory milieu, leading to aggravation of liver fibrosis. The current study provides new cautious information of LAB for liver fibrosis patients to prevent the detrimental effect of LAB supplements.

Γ-Aminobutyric acid promotes methionine-choline deficient diet-induced nonalcoholic steatohepatitis

Seok Roh, Yoon,Cho, Ara,Zhou, Zixiong,Jeong, Hyuneui,Park, Jeong-Eun,Cha, Youn-Soo,Oh, Suk-Heung,Lim, Chae-Woong,Kim, Bumseok Editorial Department of Journal of Biomedical Rese 2017 JOURNAL OF BIOMEDICAL RESEARCH -ELSEVIER- ENGLISH Vol.31 No.1

<P><B>Abstract</B></P><P>Nonalcoholic steatohepatitis (NASH) is one of the most common liver diseases and a major cause of liver fibrosis worldwide. Γ-Aminobutyric acid (GABA) is one of the most abundant inhibitory neurotransmitters in the central nervous system. Recently, it has been reported that GABAergic signaling pathways are found in various non-neuronal tissues including the immune system and play a functional role. In the present study, we investigated whether administration of GABA has effects on NASH through its immunomodulatory effects. To test this hypothesis, C57BL/6 mice were fed a methionine–choline-deficient (MCD) diet for 8 weeks. After four weeks into MCD feeding, mice were provided with plain water (control) or water containing 2 mg/mL of GABA for the subsequent 4 weeks. Using this MCD diet-induced NASH model, we found that mice receiving GABA showed more severe steatohepatitis and liver fibrosis than control mice. This increased liver damage was confirmed by higher levels of serum alanine transaminase (ALT) and aspartate aminotransferase (AST) compared to the control group. In accordance with increased liver steatohepatitis, NASH-related and inflammatory gene expression (collagen α1, tissue inhibitor of metalloproteinase-1, TNF-α) in the liver was markedly increased in GABA-treated mice. Furthermore, GABA directly enhanced production of inflammatory cytokines including IL-6 and TNF-α in LPS activated RAW macrophage cells and increased TIB–73 hepatocyte death. Such effects were abolished when GABA was treated with bicuculline, a competitive antagonist of GABA receptors. These results suggest that oral administration of GABA may be involved in changes of the liver immune milieu and conferred detrimental effects on NASH progression.</P>