http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
( Min Young Rim ),( Soo Yong Park ),( In Ku Yo ),( Min Su Ha ),( Ju Seung Kim ),( Ju Won Lee ),( Young Kul Jung ),( Dong Hae Chung ),( Oh Sang Kwon ),( Yun Soo Kim ),( Duck Joo Choi ),( Ju Hyun Kim1 ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.-
Background: Autoimmune hepatitis (AIH) is a progressive inflammatory liver disease of unknown etiology that is reported to be a consequence of aberrant autoreactivity. Several studies which reported the acute presentation of AIH have different clinical course and histologic features. In this study, we compared acute presentation of AIH and chronic presentation of AIH. Methods: We retrospectively reviewed the medical records of patients with autoimmune hepatitis from January 2003 to June 2011 at Gachon University, Gil Hospital. A total of 29 patients were enrolled, 7 patients were diagnosed with acute presentation of AIH. Results: There was no difference between two group in age, gender, and score system of AIH. Patients with acute presentation had higher serum levels of total bilirubin, lower serum levels of albumin in clinical feature (p<0.05), and higher frequency of zone 3 necrosis in histologic feature. The cumulative incidental rate of the normalization of serum AST and ALT levels with prednisolone treatment was similar between patients with acute presentation and chronic presentation in clinical course. Conclusions: Higher AST, ALT and, bilirubin were clinical specific feature, and zone 3 necrosis is a histological characteristic of autoimmune hepatitis with acute presentation.
Kim, So-Jung,Ha, Ga-Hee,Bae, Jae-Ho,Kim, Ga Rim,Son, Cheol-Hun,Park, You-Soo,Yang, Kwangmo,Oh, Sae-Ock,Kim, Sun-Hee,Kang, Chi-Dug Elsevier 2015 Experimental cell research Vol.330 No.2
<P><B>Abstract</B></P> <P>In the present study, we investigated whether celecoxib could induce the expression of NKG2D ligands in clonogenic colon cancer cells, and increase their susceptibility to NK cell-mediated cell death. Celecoxib and its non-coxib analog, 2,5-dimethyl celecoxib, induced ULBP-1 and DR5 in both COX-2 negative HCT-15 cells and COX-2 positive HT-29 cells. Celecoxib increased their susceptibility to NK92 cells in both DELFIA assay and soft agar colony forming assay. The inducibility of ULBP-1 and DR5 by celecoxib was not different between CD44- and CD44+ HCT-15 cells, and CD133- and CD133+ HT-29 cells. Celecoxib increased the susceptibility of highly clonogenic CD44+ HCT-15 and CD133+ HT-29 cells to NK92 cells, at least comparable to less clonogenic CD44- HCT-15 and CD133- HT-29 cells, respectively. In addition, celecoxib induced CHOP, and thapsigargin, an inducer of ER (endoplasmic reticulum) stress, induced DR5 but not ULBP1 in HCT-15. Taken together, these findings suggest that celecoxib induces the expression of ULBP-1 as well as DR5 in clonogenic colon cancer cells via COX-2 and ER stress-independent pathways, and increases their susceptibility to NK cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Celecoxib induced ULBP-1 and DR5 in both HCT-15 cells and HT-29 cells, and subsequently increased their susceptibility to NK92 cells. </LI> <LI> Celecoxib increased the susceptibility of highly clonogenic CD44+ HCT-15 and CD133+ HT-29 cells to NK92 cells. </LI> <LI> 2,5-Dimethyl celecoxib also induced ULBP-1 and DR5 in both HTC-15 and HT-29 cells similarly with celecoxib. </LI> <LI> Treatment of HCT-15 cells with thapsigargin, an inducer of ER (endoplasmic reticulum) stress, induced DR5, but not ULBP-1. </LI> </UL> </P>
Kim Min Ju,Hurh Joon,Kim Ha-Rim,Lee Sang-Wang,Sin Hong-Sig,Kim Sang-Jun,Noh Eun-mi,Oh Boung-Jun,Kim Seon-Young 한국미생물·생명공학회 2023 Journal of microbiology and biotechnology Vol.33 No.4
This study confirmed the change in functional composition and alcohol-induced acute liver injury in Aloe arborescens after fermentation. An acute liver injury was induced by administration of ethanol (3 g/kg/day) to C57BL/6J mice for 5 days. A fermented A. arborescens Miller leaf (FAAL) extract was orally administered 30 minutes before ethanol treatment. After fermentation, the emodin content was approximately 13 times higher than that of the raw material. FAAL extract significantly attenuated ethanol-induced aspartate aminotransferase, alanine aminotransferase, and triglyceride increases in serum and liver tissue. Histological analysis revealed that FAAL extract inhibits inflammatory cell infiltration and fat accumulation in liver tissues. The cytochrome P450 2E1, superoxide dismutase, and glutathione (GSH), which involved in alcohol-induced oxidative stress, were effectively regulated by FAAL extract in serum and liver tissues, except for GSH. FAAL also maintained the antioxidant defense system by upregulating heme oxygenase 1 and nuclear factor erythroid 2-related factor 2 protein expression. In addition, FAAL extract inhibited the decrease in alcohol dehydrogenase and aldehyde dehydrogenase activity, which promoted alcohol metabolism and prevented the activation of inflammatory response. Our results suggest that FAAL could be used as a potential therapeutic agent for ethanol-induced acute liver injury.
Optical Evaluation of MR8 Material spectacle Lens with a New Method for the Analysis of Blue Light
Ha-Rim Kim,Ju-Hyun Jeong 대한시과학회 2018 대한시과학회지 Vol.20 No.4
목적: MR8 로 제조된 안경렌즈에서 굴절력별로 나누어 투과율을 측정하여 광학적 시험 및 청광 영역을 David L.의 분석법을 적용하여 분석하였다 방법: 시중에서 판매되고 있는 MR8 로 제조된 –8.00D, -7.00D, -6.00D, -5.00D, -4.00D, -3.00D, 0.00D의 렌즈를 선정하여 UV-VIS Spectrophotometers(SolidSpec 3700)로 200~1000nm까지 5nm 간격으로 투과율을 측정하고, 청광영역(380~500nm)을 David L.의 청광분석 방법을 적용하여 분석하였다. 결과: 연구에 선정한 MR8렌즈들 모두 UV영역을 거의 모두 차단하였다. –8.00D의 렌즈가 청광영역에서 투과율 59.56%로 가장 낮게 측정되었고 또한, David L. 분석에 따른 청광영역1과 2에서 낮은 값이 측정되었다. 적외선 영역에서는 모든 렌즈의 투과율이 점진적으로 감소하였다. 그리고 시감투과율에서 평균 23.67%~26.33%의 계산값을 얻었고 –4.00D부터 점진적으로 감소하였다. 결론: David L.의 분석법을 적용하면, 청광 1영역에서는 최소 41.28%, 최대 46.60%가 측정되었으며, 청광 2영역에서는 최소 87.30%, 최대 97.55%가 측정되었다. 그리고 청광 3영역에서는 최소 86.83%, 최대 96.55%가 측정되었으며 평균 94%였다. 시감투과율에서는 측정된 렌즈 중 –3.00D렌즈가 26.33%으로 가장 높은 값이 계산되었으며, -8.00D렌즈가 23.67%으로 가장 낮은 계산 값을 얻었다. Purpose : We present a novel method for the analysis of blue light applied by the analysis method of David L. with optical experiment and blue light by measuring the transmittance by dividing it by the refractive power in the spectacle lens made by MR8. Methods : The lenses of –8.00D, -7.00D, -6.00D, -5.00D, -4.00D, -3.00D, and 0.00D manufactured by MR8 being sold in the market, were selected. The transmittance was measured at the intervals of 5 nm from 200 to 1000 nm with UV-VIS Spectrophotometers (SolidSpec 3700), and they were in range of the blue light (380 to 500 nm) analyzed by a David L.'s analysis method. Results : All of the MR8 lenses selected for this study almost completely blocked at the UV range. A lens of -8.00D was measured as the lowest transmittance of 59.56% in the blue light area and low values were measured at the blue areas 1 and 2 according to the analysis of David L.In the infrared ray area, the transmittance of all lenses gradually decreased. The average value of the luminous transmittance was 23.67% ~ 26.33% and then gradually decreased from -4.00D. Conclusion : Applying the analysis of David L., a minimum of 41.28% and a maximum of 46.60% were measured at the blue light 1 area and a minimum of 87.30% and a maximum of 97.55% were measured at the blue light 2 area. A minimum of 86.83% and a maximum of 96.55% were measured at the blue light 3 area, and the average was 94%. The luminous transmittance of the -3.00D lens was 26.33%, which was the highest, and that -8.00D was 23.67%, which was the lowest.
Kim, In‐,Gyu,Lee, Jei‐,Ha,Kim, Seo‐,Yeon,Hwang, Hai‐,Min,Kim, Tae‐,Rim,Cho, Eun‐,Wie John Wiley and Sons Inc. 2018 Cancer Science Vol.109 No.11
<P>Microenvironment, such as hypoxia common to cancer, plays a critical role in the epithelial‐to‐mesenchymal transition (EMT) program, which is a major route of cancer metastasis and confers γ‐radiation resistance to cells. Herein, we showed that transgelin 2 (TAGLN2), an actin‐binding protein, is significantly induced in hypoxic lung cancer cells and that Snail1 is simultaneously increased, which induces EMT by downregulating <I>E‐cadherin</I> expression. Forced <I>TAGLN2</I> expression induced severe cell death; however, a small population of cells surviving after forced <I>TAGLN2</I> overexpression showed γ‐radiation resistance, which might promote tumor relapse and recurrence. These surviving cells showed high metastatic activity with an increase of EMT markers including Snail1. In these cells, TAGLN2 activated the insulin‐like growth factor 1 receptor β (IGF1Rβ)/PI3K/AKT pathway by recruitment of focal adhesion kinase to the IGF1R signaling complex. Activation of the IGF1Rβ/PI3K/AKT pathway also induced inactivation of glycogen synthase kinase 3β (GSK3β), which is involved in Snail1 stabilization. Therefore, both the IGF1Rβ inhibitor (AG1024) and the PI3K inhibitor (LY294002) or AKT inactivation with MK2206 lower the cellular level of Snail1. Involvement of GSK3β was also confirmed by treatment with lithium chloride, the inducer of GSK3β phosphorylation, or MG132, the 26S proteasomal inhibitor, which also stabilized Snail1. In conclusion, the present study provides important evidence that hypoxia‐inducible TAGLN2 is involved in the selection of cancer cells with enhanced EMT properties to overcome the detrimental environment of cancer cells.</P>