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Han, Sae-Won,Jeon, Yoon Kyung,Lee, Kyung-Hun,Keam, Bhumsuk,Hwang, Pil Gyu,Oh, Do-Youn,Lee, Se-Hoon,Kim, Dong-Wan,Im, Seock-Ah,Chung, Doo Hyun,Heo, Dae Seog,Bang, Yung-Jue,Kim, Tae-You Lippincott Williams Wilkins, Inc. 2007 PHARMACOGENETICS AND GENOMICS Vol.17 No.5
OBJECTIVE: Limited availability of tumoral tissue in non-small-cell lung cancer and presence of epidermal growth factor receptor mutation-independent responses call for investigation of other molecular predictive marker of gefitinib responsiveness. Therefore, CA repeat polymorphism in intron 1 was analyzed for its association with gefitinib responsiveness together with epidermal growth factor receptor mutation in Korean patients. PATIENTS AND METHODS: For 86 advanced non-small-cell lung cancer patients treated with gefitinib, epidermal growth factor receptor mutation was analyzed by direct sequencing (exons 18–21) from tumor tissue and CA repeat polymorphism was assessed by fragment length analysis from tumor and/or normal tissue. RESULTS: CA repeat status was identical in 33 patients with matched tumor and normal tissue. CA repeat was low (sum of both alleles ≤37) in 40 (46.5%) and high (sum ≥38) in 46 (53.5%) patients. Although epidermal growth factor receptor mutation was more frequent in high CA repeat patients [17.5% (7/40) in low vs. 28.3% (13/46) in high, P=0.18], response rate was higher in low CA repeat patients [25.0% (10/40) in low vs. 13.0% (6/46) in high, P=0.16]. In multivariate analysis, low CA repeat was associated with better objective response (odds ratio 7.1, 95% confidence interval 1.2–40.8; P=0.029) and time-to-progression (hazard ratio 0.54, 95% confidence interval 0.34–0.88; P=0.014), independent of the epidermal growth factor receptor mutational status. CA repeat status was not associated with epidermal growth factor receptor expression. CONCLUSION: Low number of CA repeats in intron 1 of epidermal growth factor receptor is associated with gefitinib responsiveness in non-small-cell lung cancer patients independent of epidermal growth factor receptor mutation.
Establishment of Hepatoma Treatment Model Using Hepatoma Cell Spheroids
( Han Seul Park ),( Jae Young Jang ),( Seoung Won Jeong ),( Sae Hwan Lee ),( Sang Gyune Kim ),( Sang-woo Cha ),( Young Seok Kim ),( Young Deok Cho ),( Hong Soo Kim ),( Boo Sung Kim ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: Three dimensional (3D) spheroid cells are more closely mimic natural tissues and organs than cells grown in 2D. ``Biocompatible spheroidal hepatoma cell`` is thought to be closest model of real patient``s HCC. We have made spheroidal hepatoma cells using the proven technology and already confirmed apoptotic effect of ginsenoside Rh2 and Rg5 on 2D cells (Huh7 and Huh7.5.1). In this study, we investigate apoptotic effects of ginsenoside Rh2 and Rg5 using 3D hepatoma cell spheroids. Methods: Huh7 and Huh7.5.1 cells were maintained in culture dishes in RPMI supplemented with 10% inactivated fetal bovine serum (FBS) and DMEM supplemented with 10 % dialyzed FBS, respectively. When they reached about 80 % confluence, cells were harvested from 2-D petri-dish cultures by treatment with trypsin. These cells cultured in 1.5 % soft agarose gels for 10-14 days. After 10-14 days, 3-D hepatic structure was formed and treated with ginsenoside Rh2 (100, 200uM) and Rg5 (10, 50, 100uM) for 72h. Comparison between 2-D and 3-D models was done with microscopic and protein analysis. Results: The behaviors of 2D and 3D cells (Huh7 and Huh7.5.1, respectively) have been shown different morphologic change. 3-D culture of Huh7 and Huh7.5.1 cells had a longer survival time rather than 2-D cell model. The response to ginsenoside Rh2 and Rg5 on 3D culture systems showed a lower cell death rate compared with 2D culture systems. The expression of cleaved PARP protein was increased in both 2D and 3D cells with exposure to ginsenoside Rh2 and Rg5. Conclusions: Hepatoma cell sheroids had a longer survival time and a similar apoptotic effect compared to 2-D cell model in drug screening. It is expected to have an important role on the drug screening and treatment prediction in HCC.
( Han Seul Park ),( Jae Young Jang ),( Soung Won Jeong ),( Jeong-ju Yoo ),( Sae Hwan Lee ),( Sang Gyune Kim ),( Sang-woo Cha ),( Young Seok Kim ),( Young Deok Cho ),( Hong Soo Kim ),( So Young Jin ),( 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: Animal & cell models of hepatoma give a crucial information, not only pathogenesis of liver cancer but also therapeutic effects of various agents. In this study, we investigate therapeutic effects of ginsenoside Rh2 and Rg5 using animal & cell models of hepatoma comparing with sorafenib. Methods: Huh7 & huh7.5.1 cells were harvested from 2-D petri-dish and cultured in 1.5 % soft agarose gels for 10-14 days. After 10-14 days, 3-D hepatic structure was formed and treated with ginsenoside Rh2 (100, 200uM) and Rg5 (10, 50, 100uM) for 72h. Hep3b cells (2×10<sup>5</sup>) in matrigel were suspended in 100 μl of phosphate-buffered saline (PBS) and then injected into the flanks of BALB/C nude mouse at 6 weeks. Sorafenib (10mg/kg), ginsenoside Rh2 (100 uM) and Rg5 (100 uM) was injected to intra-peritoneum twice a week. After 4 weeks, all mice were sacrificed and tumor tissue was collected. The tissue was stained with hematoxylin and eosin and histological evaluation was conducted by blindly pathologist. Area of necrosis and vascular change in tumor tissue was calculated using the lasso tool to encircle the area in ZEN 2011 Imaging Software. Results: Both ginsenoside Rh2 and Rg5 induced cell necrosis in hepatocellular carcinoma (HCC) cell lines, and more necrosis occurred in 2D models. The expression of cleaved PARP protein was increased in both 2D and 3D cells with exposure to ginsenoside Rh2 and Rg5. The hepatocellular carcinoma was confirmed in hepatoma mouse models by H&E stain. Increased necrosis and telangiectasia were observed in mice treated with sorafenib, Rh2, and Rg5 compared to control mouse. Conclusions: Our findings provide insight into the use of xenograft mouse as models of HCC and ginsenoside Rh2 & Rg5 might be a potential treatment candidate of liver cancer.
The Inhibitory Effect of Lorcaserin on Non Alcoholic Fatty Liver Disease in Animal Model
( Han Seul Park ),( Jae Young Jang ),( Seoung Won Jeong ),( Sae Hwan Lee ),( Sang Gyune Kim ),( Sang-woo Cha ),( Young Seok Kim ),( Young Deok Cho ),( Hong Soo Kim ),( Boo Sung Kim ) 대한간학회 2016 춘·추계 학술대회 (KASL) Vol.2016 No.1
Aims: Nonalcoholic fatty liver disease (NAFLD) is characterized by a wide spectrum of liver damage spanning steatosis, nonalcoholic steatohepatitis, and liver cirrhosis. The aim of this study is to investigate the efficacy of lorcaserin on NAFLD in animal model. Methods: The leptin receptor deficient db/db mice and control mice (db/m) were fed a diet deficient in methionine and choline (MCD diet) and control diet for 8, respectively. Twenty mice were divided into 3 groups. The first group was fed a control diet without treatment and referred as the control group. The second group was administered with MCD diet +0.7% DMSO. The third group was administered with MCD diet +0.7% DMSO +5mg/ml of lorcaserin. Change of body weight was observed and blood was collected before sacrifice. After being sacrificed, the liver tissues were collected and fixed in formalin. Histological evaluation was evaluated by blindly pathologist. Results: The body weight of control mice was increased during the study, whereas feeding db/db mice MCD diets for 8 weeks significantly reduced in body weight. Lorcaserin treated group was associated with more rapid body weight loss compared with DMSO-treated controls. MCD diet induced excessive fat accumulation, inflammation, and some fibrosis. Liver enzyme and triglyceride were improved in lorcaserin-treated group compared with DMSO-treated control (DMSO vs lorcaserin: AST 411.3 ±40.26 vs 304.7 ±28.88 (U/L), ALT 544.8 ±38.7 vs 434.5 ±29.68 (U/L), triglyceride 31.8 ±2.02 vs 26 ±1.58 (mg/dL)). Liver histopathology showed that the fat accumulation and inflammatory cell infiltration were decreased in MCD diet +lorcaserin-treated mice compared with MCD diet +DMSO-treated controls. Conclusions: These results showed beneficial effects of lorcaserin against excessive fat accumulation and inflammation as well as liver enzyme. Therefore, our findings indicate that lorcaserin could be contributing to the decline of progression of nonalcoholic fatty liver disease.
Sae WOO Han,Ok Joon Kim,Youn young Jang,Won Bong Lim,Oh Won Mann,Jin Soo Park,Myung Rae Kim,Hong Ran Choi 대한구강악안면병리학회 2004 대한구강악안면병리학회지 Vol.28 No.4
μ방lt emitting diodes (LED) devices are commercially introduced as an alternative for low-Ievellaser therapy (11ι,T) , and it has several advantages over lasers such as a safe, efficient, and less-expensive altemative to treat wounds. And LED irradiation at the same biostimulatory wavelength has similar bíochemical effεαs. In the present study, to asses whether the I핑ht-emitting diode (LED) irradíation can stimulate bone regeneration, irradiated bony defects with or without grafting materials on rat calvaria were compared to corresponding nonirradiated control. Fifty male Sprague-Dawly rats weighing about 150g, were used. Factors for present study were designed as follows, 1) presence or absence of grafting materials, 2) with or without irradiation, and 3) number of irradiation. Two weeks after operation, rats were sacrifìced. Radiologic and 비stomorphologic fmdings were evaluated. Macrospically, there were no incidents of infection, dehiscence, hematoma and necrosis during study. Radiological findings showed greater radiopacity in the graft group and radiopacity increased as the number of irradiation increase. And microscopically, new bαle formation was great in the graft group and increased as the number of irradiation increase, Present study has shown that LED irradiation improved bone regeneration through radiologic and histomorphologic fmdings in rat.
RNA editing in <i>RHOQ</i> promotes invasion potential in colorectal cancer
Han, Sae-Won,Kim, Hwang-Phill,Shin, Jong-Yeon,Jeong, Eun-Goo,Lee, Won-Chul,Kim, Keon Young,Park, Sang Youn,Lee, Dae-Won,Won, Jae-Kyung,Jeong, Seung-Yong,Park, Kyu Joo,Park, Jae-Gahb,Kang, Gyeong Hoon The Rockefeller University Press 2014 The Journal of experimental medicine Vol.211 No.4
<P>RNA editing can increase RNA sequence variation without altering the DNA sequence. By comparing whole-genome and transcriptome sequence data of a rectal cancer, we found novel tumor-associated increase of RNA editing in <I>ras homologue family member Q</I> (<I>RHOQ</I>) transcripts. The adenosine-to-inosine (A-to-I) editing results in substitution of asparagine with serine at residue 136. We observed a higher level of the <I>RHOQ</I> RNA editing in tumor compared with normal tissue in colorectal cancer (CRC). The degree of RNA editing was associated with RhoQ protein activity in CRC cancer cell lines. RhoQ N136S amino acid substitution increased RhoQ activity, actin cytoskeletal reorganization, and invasion potential. <I>KRAS</I> mutation further increased the invasion potential of RhoQ N136S in vitro. Among CRC patients, recurrence was more frequently observed in patients with tumors having edited <I>RHOQ</I> transcripts and mutations in the <I>KRAS</I> gene. In summary, we show that RNA editing is another mechanism of sequence alteration that contributes to CRC progression.</P>