자외선의 조사간격이 브로일러 병아리의 볏 피부중 비타민 D₃함량에 미치는 영향

조인호,장윤환,이은택,여영수,배은경,김중달 한국축산학회 1994 한국축산학회지 Vol.36 No.1

This study was conducted to determine the content, of previtamin D₃(PreD₃), lumisterol₃(L₃), vitamin D₃(VD₃) and provitamin D₃(ProD₃) in comb skski of broiler chicks exposed to medium ware ultraviolet(UVB) lights in different interval. The broiler Hubbard line day old chicks(199 = 10 control + 3 irradiation interval × 9 elapsed time × 7 replica) were fed vitamin D deficient diet for 3 weeks in a windowless subdued light room and exposed to 297 ㎚ UVB light by 0.068 mJ/㎝-(10 min) three times in 0, 12 or 24 h interval. The comb skin were taken at 0, 6, 12, 18, 24, 48, 96, 144 or 240 h after last irradiation, and epidermis and dermis were separated. The lipid in sample was extracted by 9% ethyl acetate/hexane and purified by Sep-Pak silica catridge. The stright phase HPI-C was applied to analyze the concentration of Prop; and its photoproducts. When chicks were exposed once to UVB light for 30 min without interval, the mole % of ProD₃ in comb epidermis were 100% at control and 52.65% at 0 h after irradiation, thereafter it increased gradually to 88.17% at 240 h. PreD₃ and L₃ presented the maximum mole % at 0 h. VD₃ showed the peak value at 12 h. then decreased slowly. As UVB light was utilized to irradiate the chicks for 10 thin three times in 12 h interval, the ProD₃ mole portion in epidermis at 0 h was 76.4%, the lowest value among tested. PreD₃ and 1-3 preserved the highest level at 24 and 0 h, respectively, thereafter decreased gradully. VD₃ showed a peak at 6 h after exposure. When 24 h interval system was treated, the lowest value of ProD₃ 83.52% was appeared at 0 h. PreD₃ and L3 showed the highest level at 6 and 0 h, respectively. Mole ale of VD₃ had a peak value at 6 h and thin decreased. The mole % of ProD₃ and its photoproduets in comb dermis presented similar trends of time course variation as in those in epidermis. In respecting the method of UVB irradiation the PreD₃, L, and VDT were produced more quickly and largely in no intend system as compared to the time and amount produced in 12 or 24 h interval system.

자외선 조사간격이 브로일러 병아리 다리 피부의 비타민 D3 함량에 미치는 영향

장윤환(Y . H . Chiang),조인호(I . H . Cho),여영수(Y . S . Yeoh),이은택(E .T . Lee),배은경(E . K . Bae),김중달(J . D . Kim),M . F . Holick(M . F . Holicka) 한국영양사료학회 1993 韓國營養飼料學會誌 Vol.17 No.6

Hydrogen peroxide-responsive copolyoxalate nanoparticles for detection and therapy of ischemia-reperfusion injury

Lee, D.,Bae, S.,Ke, Q.,Lee, J.,Song, B.,Karumanchi, S.A.,Khang, G.,Choi, H.S.,Kang, P.M. Elsevier Science Publishers 2013 Journal of controlled release Vol.172 No.3

The main culprit in the pathogenesis of ischemia/reperfusion (I/R) injury is the generation of high level of hydrogen peroxide (H<SUB>2</SUB>O<SUB>2</SUB>). In this study, we report a novel diagnostic and therapeutic strategy for I/R injury based on H<SUB>2</SUB>O<SUB>2</SUB>-activatable copolyoxalate nanoparticles using a murine model of hind limb I/R injury. The nanoparticles are composed of hydroxybenzyl alcohol (HBA)-incorporating copolyoxalate (HPOX) that, in the presence of H<SUB>2</SUB>O<SUB>2</SUB>, degrades completely into three known and safe compounds, cyclohexanedimethanol, HBA and CO<SUB>2</SUB>. HPOX effectively scavenges H<SUB>2</SUB>O<SUB>2</SUB> in a dose-dependent manner and hydrolyzes to release HBA which exerts intrinsic antioxidant and anti-inflammatory activities both in vitro and in vivo models of hind limb I/R. HPOX nanoparticles loaded with fluorophore effectively and robustly image H<SUB>2</SUB>O<SUB>2</SUB> generated in hind limb I/R injury, demonstrating their potential for bioimaging of H<SUB>2</SUB>O<SUB>2</SUB>-associated diseases. Furthermore, HPOX nanoparticles loaded with anti-apoptotic drug effectively release the drug payload after I/R injury, exhibiting their effectiveness for a targeted drug delivery system for I/R injury. We anticipate that multifunctional HPOX nanoparticles have great potential as H<SUB>2</SUB>O<SUB>2</SUB> imaging agents, therapeutics and drug delivery systems for H<SUB>2</SUB>O<SUB>2</SUB>-associated diseases.

Ahnak functions as a tumor suppressor via modulation of TGFβ/Smad signaling pathway

Lee, I H,Sohn, M,Lim, H J,Yoon, S,Oh, H,Shin, S,Shin, J H,Oh, S-H,Kim, J,Lee, D K,Noh, D Y,Bae, D S,Seong, J K,Bae, Y S Macmillan Publishers Limited 2014 Oncogene Vol.33 No.38

We provide detailed mechanisms of Ahnak-mediated potentiation of transforming growth factor β (TGFβ) signaling, which leads to a negative regulation of cell growth. We show that Smad3 interacts with Ahnak through MH2 domain and that Ahnak stimulates Smad3 localization into nucleus leading to potentiating TGFβ-induced transcriptional activity of R-Smad. Moreover, overexpression of Ahnak resulted in growth retardation and cell cycle arrest through downregulation of c-Myc and cyclin D1/D2. We describe results from analyses of Ahnak<SUP>−/−</SUP> mouse model expressing middle T antigen in a mammary gland-specific manner (MMTV<SUP>Tg/+</SUP>Ahnak<SUP>−/−</SUP>), which showed significantly progressed hyperplasia of mammary glands compared with MMTV<SUP>Tg/+</SUP>Ahnak<SUP>+/+</SUP>. Finally, we screened multiple human breast cancer tissues and showed that the expression of Ahnak in cancer tissues is lower than that in control tissues by 50%. Taken together, these data indicate that Ahnak mediates a negative regulation of cell growth and acts as novel tumor suppressor through potentiation of TGFβ signaling.

Thiouracil , Thyroprotein 및 Diethylstilbestrol 의 병용처리가 웅추의 성장과 장기중량에 미치는 영향

배종하,조헌조,변명대 ( J . H . Bae . H . J . Cho,M . D . Byun ) 한국축산학회 1977 한국축산학회지 Vol.19 No.2

Eleven weeks old white leghorn male chicks with single comb were injected under the subcutaneous mear the neck with total 2㎖ of synthetic estrogen solution which contained 27㎎ of diethylstil bestrol (D.E.S.), and 3㎎ of euvestin, a derivative of D.E.S. in 1㎖ of aqueous suspension. In addition to the treatment with D.E.S., both thiouracil (0.01% in the ration) and thyroprotein (0.01% in the ration) were fed for 5 weeks, weight gains and the effect on each organs weight in these three group were compared with the control. The results are as follows 1. Statistical significance were P$lt;0.01 in body weight gains among the treatments. The hormone treatment caused growth stimulation about 20% in three injected groups but there were no significant differences between thiouracil group and thyroprotein group. 2. Weight of comb and testis was remarkably reduced (P$lt;0. Ol) by het treatment of hormone solution. Testis weight was showing no significance between neighbouring groups but comb weight showed significant differences between D.E.S. group and thyroprotein group. 3. Weight of liver showed significance with P$lt;0.01 among the each groups, and was showing no significance between the D.E.S. group and thyroprotein group. 4. The abdominal adipose leaf developed remarkably P$lt;0.01 between each group, it was the most ,striking in the D.E.S. group, followed by the thyrotein group, which was 6 times as much as the weight of the control. 5. The liver moisture content was reduced by injection of D.E.S. The liver fat content showed notable difference P$gt;0.01 among the groups and was increased in order, thiouracil, and thyroprotein group The liver fat content in the D.E.S. group was 2 times as much as the control In the muscle, fat content was Slightly increased in the D.E.S. group but no chance was shown in the other group.

MicroRNA-221 governs tumor suppressor HDAC6 to potentiate malignant progression of liver cancer

Bae, H.J.,Jung, K.H.,Eun, J.W.,Shen, Q.,Kim, H.S.,Park, S.J.,Shin, W.C.,Yang, H.D.,Park, W.S.,Lee, J.Y.,Nam, S.W. Elsevier Science Publishers 2015 Journal of hepatology Vol.63 No.2

Background & Aims: Most common reason behind changes in histone deacetylase (HDAC) function is its overexpression in cancer. However, among HDACs in liver cancer, HDAC6 is uniquely endowed with a tumor suppressor, but the mechanism underlying HDAC6 inactivation has yet to be uncovered. Methods: Microarray profiling and target prediction programs were used to identify miRNAs targeting HDAC6. A series of inhibitors, activators and siRNAs was introduced to validate regulatory mechanisms for microRNA-221-3p (miR-221) governing HDAC6 in hepatocarcinogenesis. Results: Comprehensive miRNA profiling analysis identified seven putative endogenous miRNAs that are significantly upregulated in hepatocellular carcinoma (HCC). While miR-221 was identified as a suppressor of HDAC6 by ectopic expression of miRNA mimics in Dicer knockdown cells, targeted-disruption of miR-221 repressed cancer cell growth through derepressing HDAC6 expression. Suppression of HDAC6 via miR-221 was induced by JNK/c-Jun signaling in liver cancer cells but not in normal hepatic cells. Additionally, cytokine-induced NF-κBp65 independently regulated miR-221, thereby suppressing HDAC6 expression in HCC cells. HCC tissues derived from chemical-induced rat and H-ras12V transgenic mice liver cancer models validated that JNK/c-Jun activation and NF-κBp65 nuclear translocation are essential for the transcription of miR-221 leading to repression of HDAC6 in HCC. Conclusions: Our findings suggest that the functional loss or suppression of the tumor suppressor HDAC6 is caused by induction of miR-221 through coordinated JNK/c-Jun- and NF-κB-signaling pathways during liver tumorigenesis, providing a novel target for the molecular treatment of liver malignancies.

Circulating Fluidized Bed Combustion of Korean Anthracite

Shun, D 한국화학공학회 1996 Korean Chemical Engineering Research(HWAHAK KONGHA Vol.34 No.3

Proton Implantation Mechanism in GaN Layer Transfer by Using the Ion-Cut Process

H. J Woo,C. H Eum,G. D Kim,H. W Choi,J. K Kim,W. Hong,Y. H Bae 한국물리학회 2007 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.50 No.I

The proton implantation condition for the ion-cut process in wurtzite-phase GaN and the associated mechanisms of surface blistering of GaN films were investigated. Etch-pit density (EPD) measurements, photoluminescence (PL) spectroscopy, and high resolution X-ray diffraction (HRXRD) were used to investigate the crystalline quality of the as-grown GaN epi-wafers. The proton beam was implanted at 60 keV with fluences in the range of 3 $\sim$ 5 $\times$ 10$^{17}$ H$^+$/cm$^2$ at room temperature. The influences of the crystallinity of the GaN wafers, the ion fluence and the post-implantation annealing conditions (200 $\sim$ 450 $^\circ$C) on the blistering process were studied. Optical microscopy, field emission scanning electron microscopy (FE-SEM), HRXRD, Rutherford backscattering Spectrometry (RBS)/channeling (RBS/C), and cross-sectional transmission electron microscopy (XTEM) were used to investigate splitting kinetics, and the optimum conditions for achieving exfoliation only after post-implantation annealing were determined for the GaN ion-cut process. Our results suggest that the ion-cut process is sensitive to both the implant fluence and the annealing conditions, however, so far as the measured crystal quality is concerned, against our expectations, there was no notable influence on the blistering property. The optimum post-implantation annealing temperature was less than 350 $^\circ$C, and low temperature splitting is of importance for layer transfer between dissimilar materials with very different thermal expansion coefficients.

원발성 간암에서 PIVKA-II 및 Lens Culinaris Agglutinin-A 반응성 Alpha-fetoprotein(AFP-L3)의 임상적 유용성

배시현,박두호,양진모,박영민,차상복,최종영,성광용,조세현,정규원,선희식,김부성,최상욱,변병훈,한남익 대한간학회 2000 Clinical and Molecular Hepatology(대한간학회지) Vol.6 No.2

Background/Aims: Des-γ-carboxy prothrombin(DCP), a protein induced by vitamin K absence or antagonist-II(PIVKA-II), and Lens culinaris agglutinin-A reactive AFP-L3 have been reported to be useful markers for the diagnosis of hepatocellular carcinoma (HCC). In the present study, both the PIVKA-II and AFP-L3 were analyzed and compared with a conventional AFP to determine its usefulness, specificity and sensitivity in the diagnosis of HCC. Methods: Sera were collected from 108 patients consisting of 17 patients with chronic hepatitis, 22 patients with liver cirrhosis and 69 patients with HCC. The AFP-L3 was determined by an lectin affinity electrophoresis coupled with an antibody-affinity blotting. Level of DCP was measured by an enzyme immunoassay with an anti-DCP monoclonal antibody. Results: The sensitivity and specificity of PIVKA-II and AFP L3 were 49.3% and 89.5%, and 32.5% and 85.7%, respectively. No significant correlation was found between the PIVKA-II or AFP L3 and serum AFP. No correlation was found etween the PIVKA-II or AFP L3 and the characteristics of HCC. Conclusion: The determination of plasma DCP and AFP L3 levels combined with AFP levels may be useful especially for the differential diagnosis between HCC and chronic liver diseases without HCC.(Korean J HepatoBackground/Aims: Des-γ-carboxy prothrombin(DCP), a protein induced by vitamin K absence or antagonist-II(PIVKA-II), and Lens culinaris agglutinin-A reactive AFP-L3 have been reported to be useful markers for the diagnosis of hepatocellular carcinoma (HCC). In the present study, both the PIVKA-II and AFP-L3 were analyzed and compared with a conventional AFP to determine its usefulness, specificity and sensitivity in the diagnosis of HCC. Methods: Sera were collected from 108 patients consisting of 17 patients with chronic hepatitis, 22 patients with liver cirrhosis and 69 patients with HCC. The AFP-L3 was determined by an lectin affinity electrophoresis coupled with an antibody-affinity blotting. Level of DCP was measured by an enzyme immunoassay with an anti-DCP monoclonal antibody. Results: The sensitivity and specificity of PIVKA-II and AFP-L3 were 49.3% and 89.5%, and 32.5% and 85.7%, respectively. No significant correlation was found between the PIVKA-II or AFP-L3 and serum AFP. No correlation was found etween the PIVKA-II or AFP L3 and the characteristics of HCC. Conclusion: The determination of plasma DCP and AFP-L3 levels combined with AFP levels may be useful especially for the differential diagnosis between HCC and chronic liver diseases without HCC.(Korean J Hepatol 2000;6:205-214)l 2000;6:205-214)

Phospholipase D1 regulates autophagic flux and clearance of α-synuclein aggregates

Bae, E-J,Lee, H-J,Jang, Y-H,Michael, S,Masliah, E,Min, D S,Lee, S-J Macmillan Publishers Limited 2014 CELL DEATH AND DIFFERENTIATION Vol.21 No.7

Many neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, are characterized by abnormal accumulations of aggregated proteins. Brains in these diseases also show accumulation of autophagic vesicles in the neuronal cytoplasm, suggesting impairment of the autophagic process. As autophagy involves de novo membrane production and vesicle fusion, extensive changes in lipid molecules are necessary. However, the involvement of signaling lipid-modifying enzymes in autophagy and their roles in neurodegenerative diseases are not clear. Using specific inhibitor, we show that loss of phospholipase D1 (PLD1) activity resulted in an accumulation of microtubule-associated protein light chain 3 (LC3), p62, and polyubiquitinated proteins, signs representing malfunction in autophagic flux. Fluorescence and electron microscopic analyses demonstrated impaired fusion of autophagosomes with lysosomes, resulting in accumulation of autophagosomes. Within the cells with impaired autophagic flux, α-synuclein aggregates accumulated in autophagosomes. Knockdown of PLD1 expression using small interfering RNA also resulted in impaired autophagic flux and accumulation of α-synuclein aggregates in autophagosomes. Neuronal toxicity caused by α-synuclein accumulation was rescued by overexpression of PLD1; however, expression of activity-deficient mutant, PLD1-KRM, showed reduced rescue effects. Finally, we demonstrated that both PLD activity and expression levels were reduced in brain tissues of dementia with Lewy bodies (DLB) patients, whereas the amounts of α-synuclein and p62 were increased in the same tissue samples. Collectively, these results suggest that insufficient PLD activity, and therefore, the changes in phospholipid compositions within membranes, might be an important contributor to impaired autophagic process and protein accumulation in Lewy body diseases.