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Search Results: 1 - 10 of 9355 matches for " Eun Jeong Sohn1 "
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PEP-1-p18 prevents neuronal cell death by inhibiting oxidative stress and Bax expression
Duk-Soo Kim2,#, Eun Jeong Sohn1,#, Dae Won Kim1, Young Nam Kim1, Seon Ae Eom1, Ga Hyeon Yoon1, Sung-Woo Cho3, Sang-Hyun Lee1, Hyun Sook Hwang1, Yoon Shin Cho1, Jinseu Park1, Won Sik Eum1,* & Soo Young Choi1,*
BMB Reports , 2012,
Abstract: P18, a member of the INK4 family of cyclin-dependent kinaseinhibitors, is a tumor suppressor protein and plays a key cellsurvival role in a variety of human cancers. Under pathophysiologicalconditions, the INK4 group proteins participate in novelbiological functions associated with neuronal diseases andoxidative stress. Parkinson’s disease (PD) is characterized by loss ofdopaminergic neurons, and oxidative stress is important in itspathogenesis. Therefore, we examined the effects of PEP-1-p18 onoxidative stress-induced SH-SY5Y cells and in a PD mouse model.The transduced PEP-1-p18 markedly inhibited 1-methyl-4-phenylpyridinium-induced SH-SY5Y cell death by inhibiting Baxexpression levels and DNA fragmentation. Additionally, PEP-1-p18prevented dopaminergic neuronal cell death in the substantia nigraof a 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced PDmouse model. These results indicate that PEP-1-p18 may be auseful therapeutic agent against various diseases and is a potentialtool for treating PD.
An Interesting Case of Cardiac Amyloidosis Initially Misdiagnosed as Syndrome X  [PDF]
Hyung Rae Sohn, Bong Gun Song, Eun Jin Kim, Seong Yeon Jeong, Su-Min Hong, Hyun Gul Jung, Hye-Jin Jung, Wook-Hyun Cho, Suk-Koo Choi
International Journal of Clinical Medicine (IJCM) , 2011, DOI: 10.4236/ijcm.2011.25102
Abstract: Cardiac infiltration of amyloid fibril results in progressive cardiomyopathy with a grave prognosis and results in cardiac diseases such as congestive heart disease, cardiomyopathy, valvular heart disease, and arrhythmias. We present a rare case of cardiac amyloidosis initially misdiagnosed as syndrome X in which recurrent chest pain and progressive heart failure could be managed finally by heart transplantation.
Effects of Group 1 versus Group 2 Carbapenems on the Susceptibility of Acinetobacter baumannii to Carbapenems: A Before and After Intervention Study of Carbapenem-Use Stewardship
Young Kyung Yoon, Kyung Sook Yang, Seung Eun Lee, Hyun Jeong Kim, Jang Wook Sohn, Min Ja Kim
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099101
Abstract: Objective Antimicrobial stewardship programs have been proposed for reducing bacterial resistance in the hospital environment. The purpose of this study was to investigate the impact of a carbapenem-use stewardship program on the susceptibility of Acinetobacter baumannii to Group 2 carbapenems. Methods A before and after intervention study was conducted at a university hospital from September 2008 to February 2013. Three study periods were defined: Phase I, pre-intervention (months 1–18); Phase II, a postintervention period during which ertapenem use was mandated but carbapenem use was not restricted (months 19–36); and Phase III, a postintervention period during which Group 2 carbapenem use was restricted (months 37–54). Results During the study period, intervention resulted in diminished consumption of Group 2 carbapenems (antimicrobial use density (AUD): 21.3±6.0 in Phase I, 18.8±6.0 in Phase II, 16.1±4.4 in Phase III; P = 0.028) and increased consumption of ertapenem (AUD: 2.7±1.7 in Phase I, 7.2±4.5 in Phase II, 9.1±5.3 in Phase III; P<0.001). The use of autoregressive-error models showed that in contrast with ertapenem use, the use of Group 2 carbapenem during the previous one month was positively and significantly associated with a subsequent increase in the proportion of carbapenem-resistant A. baumannii (CRAB) (P = 0.031). Conclusions Implementing a carbapenem-use stewardship program featuring the preferential use of ertapenem for treating appropriate indications of infection resulted in reduced use of Group 2 carbapenems and had a positive impact on the susceptibility of A. baumannii to carbapenems. This approach could be integrated into CRAB-control strategies in hospitals.
Inhibition of Connexin 26/43 and Extracellular-Regulated Kinase Protein Plays a Critical Role in Melatonin Facilitated Gap Junctional Intercellular Communication in Hydrogen Peroxide-Treated HaCaT Keratinocyte Cells
Hyo-Jung Lee,Hyo-Jeong Lee,Eun Jung Sohn,Eun-Ok Lee,Jin-Hyoung Kim,Min-Ho Lee,Sung-Hoon Kim
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/589365
Abstract: Though melatonin was known to regulate gap junctional intercellular communication (GJIC) in chick astrocytes and mouse hepatocytes, the underlying mechanism by melatonin was not elucidated in hydrogen peroxide- (H2O2-) treated HaCaT keratinocyte cells until now. In the current study, though melatonin at 2 mM and hydrogen peroxide (H2O2) at 300 μM showed weak cytotoxicity in HaCaT keratinocyte cells, melatonin significantly suppressed the formation of reactive oxygen species (ROS) in H2O2-treated HaCaT cells compared to untreated controls. Also, the scrape-loading dye-transfer assay revealed that melatonin enhances the intercellular communication by introducing Lucifer Yellow into H2O2-treated cells. Furthermore, melatonin significantly enhanced the expression of connexin 26 (Cx26) and connexin 43 (Cx43) at mRNA and protein levels, but not that of connexin 30 (Cx30) in H2O2-treated HaCaT cells. Of note, melatonin attenuated the phosphorylation of extracellular signal-regulated protein kinases (ERKs) more than p38 MAPK or JNK in H2O2-treated HaCaT cells. Conversely, ERK inhibitor PD98059 promoted the intercellular communication in H2O2-treated HaCaT cells. Furthermore, combined treatment of melatonin (200 μM) and vitamin C (10 μg/mL) significantly reduced ROS production in H2O2-treated HaCaT cells. Overall, these findings support the scientific evidences that melatonin facilitates gap junctional intercellular communication in H2O2-treated HaCaT keratinocyte cells via inhibition of connexin 26/43 and ERK as a potent chemopreventive agent.
Synthesis of PEG-Iodine-Capped Gold Nanoparticles and Their Contrast Enhancement in In Vitro and In Vivo for X-Ray/CT
Sun-Hee Kim,Eun-Mi Kim,Chang-Moon Lee,Dong Wook Kim,Seok Tae Lim,Myung-Hee Sohn,Hwan-Jeong Jeong
Journal of Nanomaterials , 2012, DOI: 10.1155/2012/504026
Abstract: We designed gold nanoparticles (AuNPs) capped with iodine and polyethylene glycol (PEG) to provide effective enhancement for X-ray CT imaging. The methoxy PEG-iodine-capped AuNPs were prepared through the chemisorption of iodine and substitution of methoxy PEG-SH onto the surface of gold nanoparticles, and severe aggregation in TEM was not observed. The binding energies of Au 4f7/2 and I 3d5/2 of the methoxy PEG-iodine-capped AuNPs were obtained as 84.1 eV and 619.3 eV, respectively. The binding energy shift of methoxy PEG-iodine-capped AuNPs would be resulted from the chemisorption between gold nanoparticles and iodine atoms. The methoxy PEG-iodine-capped AuNPs have higher enhancement compared to PEG-capped gold nanoparicles in the same amount of gold in vitro. After postinjection of methoxy PEG-iodine-capped AuNPs into the mice, dramatic contrast enhancement at the heart, aorta, liver, and kidney was observed, this was maintained up to 5 days, and there was no evidence of apparent toxicity. In conclusion, methoxy PEG-iodine-capped AuNPs might be a good candidate as a CT contrast agent for blood pool imaging, and this will also contribute to the prolongation of a blood circulation time for X-ray CT imaging.
The roles of FADD in extrinsic apoptosis and necroptosis
Eun-Woo Lee1,*, Jinho Seo1, Manhyung Jeong1, Sangsik Lee2 & Jaewhan Song1,*
BMB Reports , 2012,
Abstract: Fas-associated protein with death domain (FADD), an adaptorthat bridges death receptor signaling to the caspase cascade, isindispensible for the induction of extrinsic apoptotic cell death.Interest in the non-apoptotic function of FADD has greatlyincreased due to evidence that FADD-deficient mice ordominant-negative FADD transgenic mice result in embryoniclethality and an immune defect without showing apoptoticfeatures. Numerous studies have suggested that FADD regulatescell cycle progression, proliferation, and autophagy, affectingthese phenomena. Recently, programmed necrosis, also callednecroptosis, was shown to be a key mechanism that inducesembryonic lethality and an immune defect. Supporting thesefindings, FADD was shown to be involved in various necroptosismodels. In this review, we summarize the mechanism ofextrinsic apoptosis and necroptosis, and discuss the in vivo andin vitro roles of FADD in necroptosis induced by various stimuli.
Impact of de-escalation therapy on clinical outcomes for intensive care unit-acquired pneumonia
Mi Kyong Joung, Jeong-a Lee, Soo-youn Moon, Hae Cheong, Eun-Jeong Joo, Young-Eun Ha, Kyung Sohn, Seung Chung, Gee Suh, Doo Chung, Jae-Hoon Song, Kyong Peck
Critical Care , 2011, DOI: 10.1186/cc10072
Abstract: This was a retrospective observational cohort study of ICU patients who developed pneumonia more than 48 hours after admission to the ICU at Samsung Medical Center from September 2004 to December 2007.The 137 patients comprised 44 (32.1%) who received de-escalation therapy and 93 in the non-de-escalation group. The de-escalation group showed a lower pneumonia-related mortality rate than the non-de-escalation group by day 14 (2.3% vs. 10.8%, respectively; P = 0.08) and by day 30 (2.3% vs. 14%, respectively; P = 0.03) after the diagnosis of pneumonia. The variables independently associated with ICU-acquired pneumonia-related mortality included the Acute Physiology and Chronic Health Evaluation II (APACHE II) score and the modified Clinical Pulmonary Infection Score (CPIS) after 5 days with pneumonia. The non-de-escalation group had significantly higher APACHE II score and modified CPIS after 5 days with ICU-acquired pneumonia compared to the de-escalation group. Among all patients, 20.4% (28 of 137) had negative cultures for pathogens, and 42.9% (12 of 28) received de-escalation therapy. The latter 12 patients received de-escalation therapy and survived 30 days after the diagnosis of pneumonia.Patients in the de-escalation group showed a significantly lower mortality rate compared to patients in the non-de-escalation group. De-escalation therapy can be safely provided to patients with ICU-acquired pneumonia if they are clinically stable by day 5, even in those whose respiratory specimen cultures yield no specific pathogens.Nosocomial pneumonia accounts for almost one-half of all intensive care unit (ICU) mortality and approximately 60% of mortality due to all nosocomial infections. The initial choice of antimicrobial therapy is critical to the clinical outcome of patients with nosocomial pneumonia. Early and aggressive empirical therapy with broad-spectrum agents targeted at the likely pathogens has been associated with a reduction in the ventilator-associated pneumon
KIOM-79, an Inhibitor of AGEs–Protein Cross-linking, Prevents Progression of Nephropathy in Zucker Diabetic Fatty Rats
Young Sook Kim,Junghyun Kim,Chan-Sik Kim,Eun Jin Sohn,Yun Mi Lee,Il-Ha Jeong,Hyojun Kim,Dae Sik Jang,Jin Sook Kim
Evidence-Based Complementary and Alternative Medicine , 2011, DOI: 10.1093/ecam/nep078
Abstract: Advanced glycation end products (AGEs) have been implicated in the development of diabetic complications, including diabetic nephropathy. KIOM-79, an 80% ethanolic extract obtained from parched Puerariae Radix, gingered Magnolia Cortex, Glycyrrhiza Radix and Euphorbia Radix, was investigated for its effects on the development of renal disease in Zucker diabetic fatty rats, an animal model of type 2 diabetes. In vitro inhibitory effect of KIOM-79 on AGEs cross-linking was examined by enzyme-linked immunosorbent assay (ELISA). KIOM-79 (50 mg/kg/day) was given to Zucker diabetic fatty rats for 13 weeks. Body and kidney weight, blood glucose, glycated hemoglobin, urinary albumin and creatinine excretions were monitored. Kidney histopathology, collagen accumulation, fibrinogen and transforming growth factor-beta 1 (TGF-β1) expression were also examined. KIOM-79 reduced blood glucose, kidney weight, histologic renal damage and albuminuria in Zucker diabetic fatty rats. KIOM-79 prevented glomerulosclerosis, tubular degeneration, collagen deposition and podocyte apoptosis. In the renal cortex, TGF-β1, fibronectin mRNA and protein were significantly reduced by KIOM-79 treatment. KIOM-79 reduces AGEs accumulation in vivo, AGE–protein cross-linking and protein oxidation. KIOM-79 could be beneficial in preventing the progression of diabetic glomerularsclerosis in type 2 diabetic rats by attenuating AGEs deposition in the glomeruli. 1. Introduction Chronic hyperglycemia is a common feature of all forms of diabetes mellitus and accelerates non-enzymatic browning in the Maillard reaction between reducing sugars and free reactive amino groups of proteins. The irreversible formation of advanced glycation/lipoxidation end products (AGEs/ALEs) affects proteins and lipids such as hemoglobin, collagen and lipoprotein and causes damage to the kidney, eyes and blood vessels [1, 2]. Diabetic nephropathy is one of the main causes of end-stage renal disease and is characterized by proteinuria, progressive accumulation of glomerular extracellular matrix (ECM) and glomerulosclerosis. The AGEs inhibitors or cross-link breakers such as aminoguanidine (AG), pyridoxamine, LR-90 and ALT-711 (alagebrium), have been reported to attenuate various functional and structural manifestations of diabetic microvascular disease within the kidney in experimental animals [3–5]. There is no Food and Drug Administration-approved agents for the specific indication of AGEs modification to date, although these synthetic and natural compounds are in clinical and preclinical testing [2]. The Zucker fatty
Genomic Predictors for Recurrence Patterns of Hepatocellular Carcinoma: Model Derivation and Validation
Ji Hoon Kim equal contributor,Bo Hwa Sohn equal contributor,Hyun-Sung Lee,Sang-Bae Kim,Jeong Eun Yoo,Yun-Yong Park,Woojin Jeong,Sung Sook Lee,Eun Sung Park,Ahmed Kaseb,Baek Hui Kim,Wan Bae Kim,Jong Eun Yeon,Kwan Soo Byun,In-Sun Chu,Sung Soo Kim,Xin Wei Wang,Snorri S. Thorgeirsson,John M. Luk,Koo Jeong Kang,Jeonghoon Heo,Young Nyun Park,Ju-Seog Lee
PLOS Medicine , 2014, DOI: 10.1371/journal.pmed.1001770
Abstract: Background Typically observed at 2 y after surgical resection, late recurrence is a major challenge in the management of hepatocellular carcinoma (HCC). We aimed to develop a genomic predictor that can identify patients at high risk for late recurrence and assess its clinical implications. Methods and Findings Systematic analysis of gene expression data from human liver undergoing hepatic injury and regeneration revealed a 233-gene signature that was significantly associated with late recurrence of HCC. Using this signature, we developed a prognostic predictor that can identify patients at high risk of late recurrence, and tested and validated the robustness of the predictor in patients (n = 396) who underwent surgery between 1990 and 2011 at four centers (210 recurrences during a median of 3.7 y of follow-up). In multivariate analysis, this signature was the strongest risk factor for late recurrence (hazard ratio, 2.2; 95% confidence interval, 1.3–3.7; p = 0.002). In contrast, our previously developed tumor-derived 65-gene risk score was significantly associated with early recurrence (p = 0.005) but not with late recurrence (p = 0.7). In multivariate analysis, the 65-gene risk score was the strongest risk factor for very early recurrence (<1 y after surgical resection) (hazard ratio, 1.7; 95% confidence interval, 1.1–2.6; p = 0.01). The potential significance of STAT3 activation in late recurrence was predicted by gene network analysis and validated later. We also developed and validated 4- and 20-gene predictors from the full 233-gene predictor. The main limitation of the study is that most of the patients in our study were hepatitis B virus–positive. Further investigations are needed to test our prediction models in patients with different etiologies of HCC, such as hepatitis C virus. Conclusions Two independently developed predictors reflected well the differences between early and late recurrence of HCC at the molecular level and provided new biomarkers for risk stratification. Please see later in the article for the Editors' Summary
Inhibition of Hypoxia Inducible Factor Alpha and Astrocyte-Elevated Gene-1 Mediates Cryptotanshinone Exerted Antitumor Activity in Hypoxic PC-3 Cells
Hyo-Jeong Lee,Deok-Beom Jung,Eun Jung Sohn,Hanna Hyun Kim,Moon Nyeo Park,Jae-Hwan Lew,Seok Geun Lee,Bonglee Kim,Sung-Hoon Kim
Evidence-Based Complementary and Alternative Medicine , 2012, DOI: 10.1155/2012/390957
Abstract: Although cryptotanshinone (CT) was known to exert antitumor activity in several cancers, its molecular mechanism under hypoxia still remains unclear. Here, the roles of AEG-1 and HIF-1α in CT-induced antitumor activity were investigated in hypoxic PC-3 cells. CT exerted cytotoxicity against prostate cancer cells and suppressed HIF-1α accumulation and AEG-1 expression in hypoxic PC-3 cells. Also, AEG-1 was overexpressed in prostate cancer cells. Interestingly, HIF-1α siRNA transfection enhanced the cleavages of caspase-9,3, and PAPR and decreased expression of Bcl-2 and AEG1 induced by CT in hypoxic PC-3 cells. Of note, DMOG enhanced the stability of AEG-1 and HIF-1α during hypoxia. Additionally, CT significantly reduced cellular level of VEGF in PC-3 cells and disturbed tube formation of HUVECs. Consistently, ChIP assay revealed that CT inhibited the binding of HIF-1α to VEGF promoter. Furthermore, CT at 10 mg/kg suppressed the growth of PC-3 cells in BALB/c athymic nude mice by 46.4% compared to untreated control. Consistently, immunohistochemistry revealed decreased expression of Ki-67, CD34, VEGF, carbonic anhydrase IX, and AEG-1 indices in CT-treated group compared to untreated control. Overall, our findings suggest that CT exerts antitumor activity via inhibition of HIF-1α, AEG1, and VEGF as a potent chemotherapeutic agent.
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