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Search Results: 1 - 10 of 19317 matches for " Jee Hye Han "
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Celastrol, an NF-κB Inhibitor, Improves Insulin Resistance and Attenuates Renal Injury in db/db Mice
Jung Eun Kim, Mi Hwa Lee, Deok Hwa Nam, Hye Kyoung Song, Young Sun Kang, Ji Eun Lee, Hyun Wook Kim, Jin Joo Cha, Young Youl Hyun, Sang Youb Han, Kum Hyun Han, Jee Young Han, Dae Ryong Cha
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0062068
Abstract: The NF-κB pathway plays an important role in chronic inflammatory and autoimmune diseases. Recently, NF-κB has also been suggested as an important mechanism linking obesity, inflammation, and metabolic disorders. However, there is no current evidence regarding the mechanism of action of NF-κB inhibition in insulin resistance and diabetic nephropathy in type 2 diabetic animal models. We investigated the effects of the NF-κB inhibitor celastrol in db/db mice. The treatment with celastrol for 2 months significantly lowered fasting plasma glucose (FPG), HbA1C and homeostasis model assessment index (HOMA-IR) levels. Celastrol also exhibited significant decreases in body weight, kidney/body weight and adiposity. Celastrol reduced insulin resistance and lipid abnormalities and led to higher plasma adiponectin levels. Celastrol treatment also significantly mitigated lipid accumulation and oxidative stress in organs including the kidney, liver and adipose tissue. The treated group also exhibited significantly lower creatinine levels and urinary albumin excretion was markedly reduced. Celastrol treatment significantly lowered mesangial expansion and suppressed type IV collagen, PAI-1 and TGFβ1 expressions in renal tissues. Celastrol also improved abnormal lipid metabolism, oxidative stress and proinflammatory cytokine activity in the kidney. In cultured podocytes, celastrol treatment abolished saturated fatty acid-induced proinflammatory cytokine synthesis. Taken together, celastrol treatment not only improved insulin resistance, glycemic control and oxidative stress, but also improved renal functional and structural changes through both metabolic and anti-inflammatory effects in the kidney. These results suggest that targeted therapy for NF-κB may be a useful new therapeutic approach for the management of type II diabetes and diabetic nephropathy.
Clinical implications of fatty pancreas: Correlations between fatty pancreas and metabolic syndrome
Jun Seok Lee, Sang Heum Kim, Dae Won Jun, Jee Hye Han, Eun Chul Jang, Ji Young Park, Byung Kwan Son, Seong Hwan Kim, Yoon Ju Jo, Young Sook Park, Yong Soo Kim
World Journal of Gastroenterology , 2009,
Abstract: AIM: To investigate the clinical implications of lipid deposition in the pancreas (fatty pancreas).METHODS: The subjects of this study were 293 patients who had undergone abdominal computed tomography (CT) and sonography. Fatty pancreas was diagnosed by sonographic findings and subdivided into mild, moderate, and severe fatty pancreas groups comparing to the retroperitoneal fat echogenicity.RESULTS: Fatty pancreas was associated with higher levels for visceral fat, waist circumference, aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol, triglyceride, high density lipoprotein, free fatty acid, γ-GTP, insulin, and the homeostasis model assessment of insulin resistance (HOMA-IR) than the control group (P < 0.05). HOMA-IR, visceral fat, triglyceride, and ALT also tended to increase with the degree of fat deposition in the pancreas on sonography. In a multivariate logistic regression analysis, HOMA-IR, visceral fat, and ALT level were independently related to fatty pancreas after adjustment for age, body mass index, and lipid profile. The incidence of metabolic syndrome in the fatty pancreas group was significantly higher than in the control group, and the numbers of metabolic syndrome parameters were significantly higher in the fatty pancreas group (P < 0.05).CONCLUSION: Sonographic fatty pancrease showed higher insulin resistance, visceral fat area, triglyceride, and ALT levels than normal pancreases. Fatty pancreas also showed a strong correlation with metabolic syndrome.
Paraplegia by Acute Cervical Disc Herniation after Shoulder Arthroscopic Surgery in Beach-Chair Position  [PDF]
Hye Young Kim, Gang Han Jung
Open Journal of Anesthesiology (OJAnes) , 2018, DOI: 10.4236/ojanes.2018.811028
Abstract: Paraplegia after non-cervical spine surgery under general anesthesia is a rare devastating postoperative complication [1]. A patient with shoulder pain was scheduled for shoulder arthroscopy due to rotator cuff repair. Arthroscopic shoulder surgery was performed with the patient in the beach-chair. Postoperatively, patients complained the weakness of both lower leg and marked numbness and tingling in the both arms. MRI showed a herniated intervertebral disc between C6 and C7 with spinal cord compression. Despite urgent discectomy, the patient remained dysesthesia of both upper extremities for 6 months. The purpose of this report is to introduce our case with a paraplegia observed after arthroscopic shoulder surgery in beach-chair position because of acute cervical herniation.
Correction: Breast density change as a predictive surrogate for response to adjuvant endocrine therapy in hormone receptor positive breast cancer
Jisun Kim, Wonshik Han, Hyeong-Gon Moon, Soo K Ahn, Hee-Chul Shin, Jee-Man You, Sae-Won Han, Seock-Ah Im, Tae-You Kim, Hye R Koo, Jung M Chang, Nariya Cho, Woo K Moon, Dong-Young Noh
Breast Cancer Research , 2012, DOI: 10.1186/bcr3353
Abstract: The authors declare that they have no competing interests.
Breast density change as a predictive surrogate for response to adjuvant endocrine therapy in hormone receptor positive breast cancer
Jisun Kim, Wonshik Han, Hyeong-Gon Moon, Soo Ahn, Hee-Chul Shin, Jee-Man You, Sae-Won Han, Seock-Ah Im, Tae-You Kim, Hye Koo, Jung Chang, Nariya Cho, Woo Moon, Dong-Young Noh
Breast Cancer Research , 2012, DOI: 10.1186/bcr3221
Abstract: We analyzed data for 1,065 estrogen receptor (ER)-positive breast cancer patients who underwent surgery between 2003 and 2006 and received at least 2 years of ET, including tamoxifen and aromatase inhibitors. MD was measured using Cumulus software 4.0 and expressed as a percentage. MD reduction (MDR) was defined as the absolute difference in MD of mammograms taken preoperatively and 8-20 months after the start of ET.At a median follow-up of 68.8 months, the overall breast cancer recurrence rate was 7.5% (80/1065). Mean MDR was 5.9% (range, -17.2% to 36.9%). Logistic regression analysis showed that age < 50 years, high preoperative MD, and long interval between start of ET to follow-up mammogram were significantly associated with larger MDR (p < 0.05). In a survival analysis, tumor size, lymph node positivity, high Ki-67 (≥ 10%), and low MDR were independent factors significantly associated with recurrence-free survival (p < 0.05). Compared with the group showing the greatest MDR (≥ 10%), the hazard ratios for MDRs of 5-10%, 0-5%, and < 0% were 1.33, 1.92, and 2.26, respectively.MD change during short-term use of adjuvant ET was a significant predictor of long-term recurrence in women with ER-positive breast cancer. Effective treatment strategies are urgently needed in patients with low MDR despite about 1 year of ET.Adjuvant endocrine therapy is the most effective systemic treatment modality for patients with hormone receptor (ER)-positive breast cancer, although many patients experience tumor recurrence during or after completion of endocrine therapy. Identifying factors that can predict disease recurrence early during adjuvant treatment may result in a more tailored strategy for patients likely to be endocrine resistant and may improve their overall outcomes.Mammographic breast density (MD) is defined by the relative proportion of radiopaque areas, indicating the presence of fibroglandular tissue among the surrounding fatty component of the breast. High MD is asso
Different metastatic pattern according to the KRAS mutational status and site-specific discordance of KRAS status in patients with colorectal cancer
Kim Mi-Jung,Lee Hye,Kim Jee,Kim Yu
BMC Cancer , 2012, DOI: 10.1186/1471-2407-12-347
Abstract: Background We evaluated the association between a KRAS mutational status and various clinicopathologic features including the metastatic pattern in patients with metastatic or recurrent colorectal cancer (MRCRC). The concordance rates of the KRAS status between primary tumor sites and paired metastatic organs were also analyzed. Methods The KRAS mutational status in codons 12, 13, and 61 from formalin-fixed sections of both primary tumors and related metastases was determined by sequencing analysis. One hundred forty-three Korean patients with MRCRC with available tissues (resection or biopsy) from both primary tumors and related metastatic sites were consecutively enrolled. Results The KRAS mutation rate was 52.4% (75/143) when considering both the primary and metastatic sites. When the relationship between the KRAS status and initial metastatic sites at the time of diagnosis of MRCRC was analyzed, lung metastasis was more frequent as the initial metastatic site in patients with the KRAS mutation than in patients without the KRAS mutation (45.3% vs. 22.1%; P = 0.003). However, liver (37.3% vs. 70.6%; P < 0.001) or distant lymph node metastases (6.7% vs. 19.1%; P = 0.025) were less frequent as the initial metastatic organ in patients with the KRAS mutation than in patients without the KRAS mutation. The discordance rate of KRAS mutational status between primary and paired metastatic sites other than the lung was 12.3% (13/106). Compared with primary tumor sites, the KRAS discordance rate was significantly higher in matched lung metastases [32.4% (12/37)] than in other matched metastatic organs (P = 0.005). Conclusions Organs initially involved by distant metastasis were different according to the KRAS mutational status in MRCRC patients. The concordance rate (87.7%) of the KRAS mutation status at metastatic sites other than the lung was generally high compared with primary tumor sites; however, lung metastasis had a high rate of KRAS discordance (32.4%).
Silibinin Suppresses TNF-α-Induced MMP-9 Expression in Gastric Cancer Cells through Inhibition of the MAPK Pathway
Sangmin Kim,Min Gew Choi,Hye Sook Lee,Se Kyung Lee,Sung Hoon Kim,Wan Wook Kim,Sung Mo Hur,Jung-Han Kim,Jun-Ho Choe,Seok Jin Nam,Jung-Hyun Yang,Sung Kim,Jeong Eon Lee,Jee Soo Kim
Molecules , 2009, DOI: 10.3390/molecules14114300
Abstract: Tumor necrosis factor (TNF)-α is one of the pro-inflammatory cytokines highly expressed in Helicobacter pylori that inhibits gastric acid secretion. In this study we determined the effect of silibinin on TNF-α-induced MMP-9 expression in gastric cancer cell lines. MMP-9 mRNA and protein expression was dose-dependently increased by TNF-α in SNU216 and SNU668 gastric cancer cells. On the other hand, TNF-α-induced MMP-9 expression was dose-dependently suppressed by silibinin. To verify the regulatory mechanism of silibinin on TNF-α-induced MMP-9 expression, the gastric cancer cell lines were pretreated with silibinin prior to TNF-α. TNF-α-induced MMP-9 expression was inhibited by the MEK1/2 specific inhibitor, UO126. Finally, we investigated the effect of adenoviral constitutively active (CA)-MEK and CA-Akt on MMP-9 expression. The expression of MMP-9 was significantly increased by CA-MEK overexpression, but not by CA-Akt overexpression. Taken together, we suggest that silibinin down-regulates TNF-α- induced MMP-9 expression through inhibition of the MEK/ERK pathway in gastric cancer cells.
Modified FOLFOX-6 chemotherapy in advanced gastric cancer: Results of phase II study and comprehensive analysis of polymorphisms as a predictive and prognostic marker
Bhumsuk Keam, Seock-Ah Im, Sae-Won Han, Hye Ham, Min A Kim, Do-Youn Oh, Se-Hoon Lee, Jee Kim, Dong-Wan Kim, Tae-You Kim, Dae Heo, Woo Kim, Yung-Jue Bang
BMC Cancer , 2008, DOI: 10.1186/1471-2407-8-148
Abstract: Seventy-three patients were administered a 2 hour infusion of oxaliplatin (100 mg/m2) and folinic acid (100 mg/m2) followed by a 46 hour continuous infusion of 5-FU (2,400 mg/m2). Genomic DNA from the patients' peripheral blood mononuclear cells was extracted. Ten polymorphisms within five genes were investigated including TS, GSTP, ERCC, XPD and XRCC.The overall response rate (RR) was 43.8%. Median time to progression (TTP) and overall survival (OS) were 6.0 months and 12.6 months, respectively. Toxicities were generally tolerable and manageable. The RR was significantly higher in patients with a 6-bp deletion homozygote (-6 bp/-6 bp) in TS-3'UTR (55.0% vs. 30.3% in +6 bp/+6 bp or +6 bp/-6 bp, p = 0.034), and C/A or A/A in XPD156 (52.0% vs. 26.1% in C/C, p = 0.038). The -6 bp/-6 bp in TS-3'UTR was significantly associated with a prolonged TTP and OS. In a multivariate analysis, the 6-bp deletion in TS-3'UTR was identified as an independent prognostic marker of TTP (hazard ratio = 0.561, p = 0.032).Modified FOLFOX-6 chemotherapy appears to be active and well tolerated as first line chemotherapy in AGC patients. The 6-bp deletion in TS-3'UTR might be a candidate to select patients who are likely to benefit from 5-FU based modified FOLFOX-6 in future large scale trial.Despite improvements in the early detection of gastric cancer, a significant proportion of patients present with inoperable stages where chemotherapy is required. 5-fluorouracil (5-FU) remains the main chemotherapeutic agent for the treatment of gastric cancer, and combination chemotherapy with 5-FU has shown an improved clinical outcomes [1]. 5-FU with cisplatin showed an effective clinical outcome [2], however, toxicities were considerable [1]. Oxaliplatin, another platinum based agent, has a more favorable tolerability profile than cisplatin. Hence, a combination chemotherapy of 5-FU with oxaliplatin has been investigated in numerous phase II studies, using different doses and schedules [3-7]. However
Carriage of the V279F Null Allele within the Gene Encoding Lp-PLA2 Is Protective from Coronary Artery Disease in South Korean Males
Yangsoo Jang,Dawn Waterworth,Jong-Eun Lee,Kijoung Song,Sujin Kim,Hyo-Soo Kim,Kyung Woo Park,Hyun-Jai Cho,Il-Young Oh,Jeong Euy Park,Bok-Soo Lee,Hyo Jeong Ku,Dong-Jik Shin,Jong Ho Lee,Sun Ha Jee,Bok-Ghee Han,Hye-Yoon Jang,Eun-Young Cho,Patrick Vallance,John Whittaker,Lon Cardon,Vincent Mooser
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018208
Abstract: The Asia-specific PLA2G7 994G-T transversion leads to V279F substitution within the lipoprotein-associated phospholipase-A2 (Lp-PLA2) and to absence of enzyme activity in plasma. This variant offers a unique natural experiment to assess the role of Lp-PLA2 in the pathogenesis of coronary artery disease (CAD) in humans. Given conflicting results from mostly small studies, a large two-stage case-control study was warranted.
5, 8, 11, 14-eicosatetraynoic acid suppresses CCL2/MCP-1 expression in IFN-γ-stimulated astrocytes by increasing MAPK phosphatase-1 mRNA stability
Jee Lee, Hyunmi Kim, Joo Woo, Eun-hye Joe, Ilo Jou
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-34
Abstract: To determine the effect of ETYA, primary cultured rat astrocytes and microglia were stimulated with IFN-γ in the presence of ETYA and then, expression of CCL2/MCP-1 and MAPK phosphatase (MKP-1) were determined using RT-PCR and ELISA. MKP-1 mRNA stability was evaluated by treating actinomycin D. The effect of MKP-1 and human antigen R (HuR) was analyzed by using specific siRNA transfection system. The localization of HuR was analyzed by immunocytochemistry and subcellular fractionation experiment.We found that ETYA suppressed CCL2/MCP-1 transcription and secretion of CCL2/MCP-1 protein through up-regulation of MKP-1mRNA levels, resulting in suppression of c-Jun N-terminal kinase (JNK) phosphorylation and activator protein 1 (AP1) activity in IFN-γ-stimulated brain glial cells. Moreover, these effects of ETYA were independent of PPAR-α. Experiments using actinomycin D revealed that the ETYA-induced increase in MKP-1 mRNA levels reflected an increase in transcript stability. Knockdown experiments using small interfering RNA demonstrated that this increase in MKP-1 mRNA stability depended on HuR, an RNA-binding protein known to promote enhanced mRNA stability. Furthermore, ETYA-induced, HuR-mediated mRNA stabilization resulted from HuR-MKP-1 nucleocytoplasmic translocation, which served to protect MKP-1 mRNA from the mRNA degradation machinery.ETYA induces MKP-1 through HuR at the post-transcriptional level in a receptor-independent manner. The mechanism revealed here suggests eicosanoids as potential therapeutic modulators of inflammation that act through a novel target.Inflammatory responses in the brain contribute to the pathogenesis of neurodegenerative disease, such as Alzheimer's disease, multiple sclerosis, and brain ischemia [1-4]. These responses are characterized by a sequential process involving the release of pro-inflammatory cytokines, increased expression of endothelial adhesion molecules and chemotactic factors, and activation of brain immune effector cel
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