Time filter

Source Type

Kim H.S.,Brain Korea 21 Project for Medical Science | Kim H.S.,Anesthesia and Pain Research Institute | Cho J.E.,Yonsei University | Hong S.W.,Kyungpook National University | And 5 more authors.
Physiological Research | Year: 2010

Remifentanil is a commonly used opioid in anesthesia with cardioprotective effect in ischemia-reperfused (I/R) heart. We evaluated the influence of remifentanil on myocardial infarct size and expressions of proteins involved in apoptosis in I/R rat heart following various time protocols of remifentanil administration. Artificially ventilated anesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. Rats were randomly assigned to one of five groups; Sham, I/R only, remifentanil preconditioning, postconditioning and continuous infusion group. Myocardial infarct size, the phosphorylation of ERK1/2, Bcl2, Bax and cytochrome c and the expression of genes influencing Ca2+ homeostasis were assessed. In remifentanil-administered rat hearts, regardless of the timing and duration of administration, infarct size was consistently reduced compared to I/R only rats. Remifentanil improved expression of ERK 1/2 and anti-apoptotic protein Bcl2, and expression of sarcoplasmic reticulum genes which were significantly reduced in the I/R rats only. Remifentanil reduced expression of pro-apoptotic protein, Bax and cytochrome c. These suggested that remifentanil produced cardioprotective effect by preserving the expression of proteins involved in anti-apoptotic pathways, and the expression of sarcoplasmic reticulum genes in I/R rat heart, regardless of the timing of administration. © 2010 Institute of Physiology v.v.i., Academy of Sciences of the Czech Republic. Source

Kim S.U.,Yonsei University | Kim D.Y.,Yonsei University | Park J.Y.,Yonsei University | Lee J.H.,Yonsei University | And 9 more authors.
Journal of Clinical Gastroenterology | Year: 2010

Goal: This study aimed to enhance the diagnostic accuracy by defining different cutoff liver stiffness measurement (LSM) values according to alanine aminotransferase (ALT) level and combining LSM with noninvasive models in patients with chronic hepatitis B (CHB). Background: Several studies have indicated that ALT influences LSM using FibroScan. Study: The study prospectively enrolled 200 patients (143 men, mean age 45.4y) between June 2007 and November 2008 who had been diagnosed with CHB and underwent both liver biopsy and LSM on the same day. Results: The area under the receiver operating characteristic curves (AUROC) of LSM for predicting cirrhosis in patients with ALT ≤upper limit of normal (ULN) was higher than that of all patients or those with ALT >ULN and ≤2× ULN (AUROC=0.884 vs. 0.849 and 0.867). The cutoff LSM values for ≥F2, ≥F3, and F4 were 6.0, 7.5, and 10.1kPa, respectively, in patients with ALT ≤ULN, whereas they were 8.9, 11.0, and 15.5kPa, respectively, in those with ALT >ULN and ≤2× ULN. The combination of LSM and the age-spleen-platelet ratio index performed the best at predicting cirrhosis, regardless of ALT level (AUROC=0.917 in patients with ALT ≤ULN, 0.909 in those with ALT ≤2× ULN, and 0.894 in all patients). Conclusions: Different cutoff LSM values according to ALT level and combination with age-spleen-platelet ratio index can enhance the performance of LSM in CHB, regardless of ALT level. Copyright © 2009 by Lippincott Williams & Wilkins. Source

Lee J.Y.,Brain Korea 21 Project for Medical Science | Moon J.H.,Yonsei University | Park J.S.,Yonsei University | Lee B.-W.,Yonsei University | And 5 more authors.
Diabetes and Metabolism Journal | Year: 2011

Background: Non-alcoholic fatty liver disease (NAFLD) is increasingly recognized as a major cause of liver-related morbidity and mortality. The underlying mechanisms of disease progression remain poorly understood, and primary therapy of NAFLD is not yet established. We investigated the effects of dietary oleate on the development and progression of NAFLD in a methionine- and choline-deficient (MCD) diet-fed animal model. Methods: A total of 30 C57BL/6J mice were randomly divided into three groups (n=10 in each group) and fed various experimental diets for four weeks: chow, MCD diet, or OMCD (MCD diet with oleate, 0.5 mg/g/day). Liver samples were examined for steatohepatitis and fibrosis parameters and associated genes. Results: Additional dietary oleate dramatically reduced MCD diet-induced hepatic steatosis. Hepatic carbohydrate responsive element-binding protein was overexpressed in MCD diet-fed mice, and dietary oleate prevented this overexpression (P<0.001). Dietary oleate partially prevented MCD diet-induced serum level increases in aspartate aminotransferase and alanine aminotransferase (P<0.001, respectively). The mRNA expressions of hepatic monocyte chemoattractant protein 1, tumor necrosis factor-α and matrix metalloproteinase-9 were increased in MCD diet-fed mice, and this overexpression of inflammatory molecules was prevented by dietary oleate (P<0.001). Hepatic pericellular fibrosis was observed in MCD diet-fed mice, and dietary oleate prevented this fibrosis. Altogether, dietary oleate prevented MCD diet-induced hepatic steatosis, inflammation and fibrosis. Conclusion: Dietary oleate has beneficial effects in every step of NAFLD development and progression and could be a nutritional option for NAFLD prevention and treatment. © 2011 Korean Diabetes Association. Source

Baatarkhuu O.,Yonsei University | Kim D.Y.,Yonsei University | Nymadawa P.,Ulaanbaatar University | Kim S.U.,Ulaanbaatar University | And 8 more authors.
Hepatology International | Year: 2012

Purpose Hepatocellular carcinoma (HCC) is the most common cancer in Mongolia. We aimed to investigate the clinical features, therapeutic modalities, overall survival and prognostic factors for Mongolian patients with HCC. Method One hundred ninety-five patients with HCC were consecutively enroled in our study. Results The mean age was 61.7 years. The most common etiology for HCC was HCV infection (n = 89, 45.6%), followed by HBV infection (n = 67, 34.4%). The mean tumor diameter was 6.0 ± 2.6 cm. Only 29 (14.9%) patients had a single lesion, while 39 (20.2%) had[3 lesions. Extrahepatic metastasis to lung (n = 23), bone (n = 10) and lymph node (n = 3) were detected in 36 (18.5%) patients. Most patients had advanced HCC-88 (45.1%) in stage III and 57 (29.2%) in stage IV. Surgical resection was performed in 27 (13.8%) patients,RFAin 23 (11.8%) andTACEin 107 (54.9%).When all the patients were categorized as 'treated' (n = 156) and 'not treated' (n = 39), the 3-year survival was significantly lower in the 'not treated' group than in the 'treated' group (11 vs. 0%, P<0.001). Tumor diameter (≥3 cm vs. C3 cm), extrahepatic metastasis, TNM stage (I/II vs. III/IV) and treatment (or supportive care) were selected as independent predictors for survival. Conclusions High proportion of patients with HCC in Mongolia is diagnosed at an advanced stage and survival of these patients is lower compared to other countries. A surveillance system and referral policy for high-risk groups should be urgently established and implemented in Mongolia. © Asian Pacific Association for the Study of the Liver 2011. Source

Wang H.J.,Brain Korea 21 Project for Medical Science | Lee E.Y.,Yonsei University | Han S.J.,Ajou University | Kim S.H.,Yonsei University | And 7 more authors.
Metabolism: Clinical and Experimental | Year: 2012

Reactive oxygen species (ROS), driven by excessive levels of glucose and free fatty acids, appears to induce cell apoptosis. However, the underlying molecular mechanism of this process remains unclear in cardiac myocytes. We investigated the glucolipotoxicity effects of high glucose and palmitic acid (C16:0) on the rat cardiomyoblast cell line (H9c2) focusing on tumor suppressor p53. Cultured H9c2 rat cardiomyoblasts were exposed to palmitate and /or to an elevated glucose concentration for 18 hours. Only the glucolipotoxic condition of 30 mM glucose in combination with 250μM palmitate resulted in significant generation of ROS and upregulation of p53 which caused to an increased cleavage of caspase-3. On the other hand, the expression of NF-E2-related factor 2 (Nrf2) showed increased tendency while the expression of NAD(P)H: quinone oxidoreductase-1 (NQO1) was decreased. N-acetyl L cysteins and pifithrin-α, an inhibitor of p53 abrogated glucolipotoxicity-induced ROS generation and p53 expression. Chromatin immunoprecipitation analysis revealed that p53 interacted antioxidant responsive elements (ARE)-containing promoter of NQO1. Upregulated p53 counteracted the Nrf2-induced transcription of ARE-containing promoter of NQO1 gene and leaded to decrease in NQO1 expression. We demonstrated that the elevated p53 mediated glucolipotoxicity-induced apoptosis of rat cardiomyoblast cell through dual pathways: stimulating pro-apoptosis signaling as well as suppressing anti-apoptosis pathway of Nrf2-NQO1 signaling. © 2012 Elsevier Inc. All rights reserved. Source

Discover hidden collaborations