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Search Results: 1 - 10 of 20459 matches for " Sunghee Kim "
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Trends of Noninvasive Radiofrequency and Minimally Invasive Treatment for the Management of Facial Aging  [PDF]
Sunghee Kim, Moonjong Kim
Journal of Cosmetics, Dermatological Sciences and Applications (JCDSA) , 2019, DOI: 10.4236/jcdsa.2019.91003
Abstract: Various treatments for the management of facial aging have been performed among which noninvasive radio-frequency (RF; i.e., thermage) treatment and minimally invasive treatments are on the rise. The purpose of this study was to analyze trends of the treatment of facial aging in Korea and to investigate relationships between the use of noninvasive RF and minimally invasive treatments. A retrospective analysis conducted on data from 4021 patients showed that thermage treatment increased by 134.9% over 5 years. As a person ages, the rate of facial treatment with both the botulinum toxin (for the masseter and lines of the glabella, lateral canthus, and forehead) and the PDO thread lift increases. The use of the treatments, nasolabial fold filler and Silhouette Soft Thread, however, was not associated with aging. The patients receiving thermage treatment were less likely to undergo any of the other treatments including PDO thread lift, Silhouette Soft Thread, nasolabial fold filler, or any of the botulinum toxin treatments. Overall, the results showed that patients who had received noninvasive RF tended to receive less minimally invasive treatment.
Associations between Pneumococcal Vaccinationand Adverse Outcomes in Patients with Suspected Acute Coronary Syndrome  [PDF]
Maliha Zahid, Ish Singla, Chester B. Good, Roslyn A. Stone, Sunghee Kim, Michael J. Fine, Ali F. Sonel
Advances in Infectious Diseases (AID) , 2012, DOI: 10.4236/aid.2012.24021
Abstract: Background: Although pneumococcal vaccination prevents the most common pneumonia of bacterial etiology, its associations without comes of Acute Coronary Syndrome (ACS) are unknown. Methods: This is a prospective cohort study of 1436 patients hospitalized with suspected ACS/non-ST elevation MI that were eligible for pneumococcal vaccination. Primary outcomes were death and subsequent Myocardial Infarction (MI) within 6-months of the index hospitalization. We used Cox regression to assess associations between pneumococcal vaccination and outcomes, adjusting for influenza vaccination and relevant clinical covariates. We also utilized propensity scores to adjust for potential confounding. Results: Overall, 937 (65.3%) patients received pneumococcal vaccination either prior to or during the index hospitalization. Unvaccinated patients had higher mortality (26.9% vs. 7.9%; p < 0.001) and non-significantly higher frequency of subsequent MI (7.4% vs. 3.5%; p = 0.06).Compared to patients who did not receive either pneumococcal or influenza vaccination, the unadjusted Hazard Ratio (HR) of death was significantly lower for those who received only pneumococcal vaccination (HR = 0.13; 95% CI 0.07 - 0.23) or both vaccinations (HR = 0.66, 95% CI 0.47 - 0.92), and significantly higher for patients who received only influenza vaccination (HR = 1.88, 95% CI 1.33 - 2.64). The corresponding HRs and 95% CIs for subsequent MI were 0.58 (95% CI 0.32 - 1.03) for pneumococcal vaccination only, 0.41 (95% CI 0.21 - 0.80) for both vaccinations and 0.97 (95% CI 0.48 - 1.95) for influenza vaccination alone. These remained unchanged after covariate or propensity score adjustment. Conclusions: Among patients hospitalized with suspected ACS, pneumococcal vaccination, with or without influenza vaccination, was associated with significantly lower risk of mortality within 6 months.
A role for spleen monocytes in post-ischemic brain inflammation and injury
Yi Bao, Eunhee Kim, Sangram Bhosle, Heeral Mehta, Sunghee Cho
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-92
Abstract: Ischemia-reperfusion causes inflammation that attracts monocyte/macrophage cells to infarct [1-3]. Monocytes are circulating antigen-presenting leukocytes that play an important role in inflammation, T-cell differentiation, phagocytosis, and innate immunity [4,5]. It has been shown that circulating and spleen monocytes are similar in their morphology, phagocytic capability, and gene expression profiles [6]. The study also identified the spleen as a monocyte reservoir and their numbers in the spleen are several folds higher than in circulation [6]. In addition, the number of monocytes that migrate to the infarct area after a myocardial infarction well exceeds the number in circulation under homeostatic conditions [4]. These studies suggest a potential role of the spleen in deploying monocytes upon cerebral ischemia.Human and mouse monocytes exhibit distinct subsets that are reminiscent of macrophage phenotypes [5,7,8]. In mice, the subset that expresses a high level of the hematopoietic cell differentiation antigen Ly-6C (Ly-6Chi) also expresses the G-protein linked membrane protein, CCR2. The Ly-6Chi/CCR2+ monocyte subset is specifically recruited to an injury site by monocyte chemoattractant protein-1 (MCP-1), which is produced by the inflamed tissue, and become classically activated M1 macrophages. In contrast, the Ly-6Clow monocyte subset expresses CX3CR1, a receptor for the chemokine CX3CL1 (fractalkine), but is devoid of CCR2 expression. This anti-inflammatory Ly-6Clow/CCR2-/CX3CR1+ subset is recruited to normal tissue and develops into resident M2 macrophages that function in host defense and repair after injury [9,10]. Recruitment of the pro-inflammatory Ly-6Chi/CCR2+ subset to inflammatory sites is believed to be CCR2-dependent, since monocytes from CCR2-null mice do not traffic as efficiently into a myocardial infarct as CCR2+ monocytes [6]. Furthermore, CCR2-null mice were protective against cerebral inflammation following ischemia [11], suggesting that CC
Proton Pump Inhibitors Exert Anti-Allergic Effects by Reducing TCTP Secretion
Sunghee Choi,Hyun Jung Min,Miyoung Kim,Eun Sook Hwang,Kyunglim Lee
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0005732
Abstract: Extracellular translationally controlled tumor protein (TCTP) is known to play a role in human allergic responses. TCTP has been identified outside of macrophages, in activated mononuclear cells, and in biological fluids from allergic patients. Even TCTP devoid of signal sequences, is secreted to extracellular environment by an yet undefined mechanism. This study is aimed at understanding the mechanism of TCTP release and its regulation. A secondary goal is to see if inhibitors of TCTP release can serve as potential anti-allergic asthmatic drugs.
Kaon BSM B-parameters using improved staggered fermions from $N_f=2+1$ unquenched QCD
Yong-Chull Jang,Chulwoo Jung,Hwancheol Jeong,Jangho Kim,Jongjeong Kim,Sunghee Kim,Weonjong Lee,Jaehoon Leem,Jeonghwan Pak,Sungwoo Park,Stephen R. Sharpe,Boram Yoon
Physics , 2015,
Abstract: We present results for the matrix elements of the additional $\Delta S=2$ operators that appear in models of physics beyond the Standard Model (BSM), expressed in terms of four BSM $B$-parameters. Combined with experimental results for $\Delta M_K$ and $\epsilon_K$, these constrain the parameters of BSM models. We use improved staggered fermions, with valence HYP-smeared quarks and $N_f=2+1$ flavors of "asqtad" sea quarks. The configurations have been generated by the MILC collaboration. The matching between lattice and continuum four-fermion operators and bilinears is done perturbatively at one-loop order. We use three lattice spacings for the continuum extrapolation: $a\approx 0.09$, $0.06$ and $0.045\;$fm. Valence light-quark masses range down to $\approx m_s^{\rm phys}/13$ while the light sea-quark masses range down to $\approx m_s^{\rm phys}/20$. Compared to our previous published work, we have added four additional lattice ensembles, leading to better controlled extrapolations in the lattice spacing and sea-quark masses. We report final results for two renormalization scales, $\mu=2\;\text{GeV}$ and $3\;\text{GeV}$, and compare them to those obtained by other collaborations. Agreement is found for two of the four BSM $B$-parameters ($B_2$ and $B_3^\text{SUSY}$). The other two ($B_4$ and $B_5$) differ significantly from those obtained using RI-MOM renormalization as an intermediate scheme, but are in agreement with recent preliminary results obtained by the RBC-UKQCD collaboration using RI-SMOM intermediate schemes.
Kaon $B$-parameter from improved staggered fermions in $N_f=2+1$ QCD
Taegil Bae,Yong-Chull Jang,Chulwoo Jung,Hyung-Jin Kim,Jangho Kim,Jongjeong Kim,Kwangwoo Kim,Sunghee Kim,Weonjong Lee,Stephen R. Sharpe,Boram Yoon,SWME Collaboration
Physics , 2011, DOI: 10.1103/PhysRevLett.109.041601
Abstract: We present a calculation of the kaon $B$-parameter, $B_K$, using lattice QCD. We use improved staggered valence and sea fermions, the latter generated by the MILC collaboration with $N_f=2+1$ light flavors. To control discretization errors, we use four different lattice spacings ranging down to $a\approx 0.045\;$fm. The chiral and continuum extrapolations are done using SU(2) staggered chiral perturbation theory. Our final result is $\hat{B}_K = 0.727 \pm 0.004 (\text{stat}) \pm 0.038 (\text{sys})$, where the dominant systematic error is from our use of truncated (one-loop) matching factors.
Neutral kaon mixing from new physics: matrix elements in $N_f=2+1$ QCD
Taegil Bae,Yong-Chull Jang,Hwancheol Jeong,Chulwoo Jung,Hyung-Jin Kim,Jangho Kim,Jongjeong Kim,Kwangwoo Kim,Sunghee Kim,Weonjong Lee,Jaehoon Leem,Stephen R. Sharpe,Boram Yoon,SWME Collaboration
Physics , 2013, DOI: 10.1103/PhysRevD.88.071503
Abstract: We present results for matrix elements of $\Delta S=2$ four-fermion operators arising generically in models of new physics. These are needed to constrain such models using the measured values of $\varepsilon_K$ and $\Delta M_K$. We use lattice QCD with 2+1 flavors of improved staggered fermions on lattices generated by the MILC collaboration. We extrapolate to the continuum from three lattice spacings ranging down to $a\approx 0.045\;$fm. Total errors are $\sim 5-6%$, arising primarily from our use of one-loop matching between lattice and continuum operators. For two of the matrix elements, our results disagree significantly from those obtained using different fermion discretizations.
Improved determination of $B_K$ with staggered quarks
Taegil Bae,Yong-Chull Jang,Hwancheol Jeong,Chulwoo Jung,Hyung-Jin Kim,Jangho Kim,Jongjeong Kim,Kwangwoo Kim,Sunghee Kim,Weonjong Lee,Jaehoon Leem,Jeonghwan Pak,Sungwoo Park,Stephen R. Sharpe,Boram Yoon
Physics , 2014, DOI: 10.1103/PhysRevD.89.074504
Abstract: We present results for the kaon mixing parameter $B_K$ obtained using improved staggered fermions on a much enlarged set of MILC asqtad lattices. Compared to our previous publication, which was based largely on a single ensemble at each of the three lattice spacings $a\approx 0.09\;$fm, $0.06\;$fm and $0.045\;$fm, we have added seven new fine and four new superfine ensembles, with a range of values of the light and strange sea-quark masses. We have also increased the number of measurements on one of the original ensembles. This allows us to do controlled extrapolations in the light and strange sea-quark masses, which we do simultaneously with the continuum extrapolation. This reduces the extrapolation error and improves the reliability of our error estimates. Our final result is $\hat{B}_K = 0.7379 \pm 0.0047 (\text{stat}) \pm 0.0365 (\text{sys})$.
Reduction of Decoy Receptor 3 Enhances TRAIL-Mediated Apoptosis in Pancreatic Cancer
Wei Wang, Mei Zhang, Weimin Sun, Shanmin Yang, Ying Su, Hengshan Zhang, Chaomei Liu, Xinfeng Li, Ling Lin, Sunghee Kim, Paul Okunieff, Zhenhuan Zhang, Lurong Zhang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0074272
Abstract: Most human pancreatic cancer cells are resistant to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. However, the mechanisms by which pancreatic cancer cells utilize their extracellular molecules to counteract the proapoptotic signaling mediated by the TNF family are largely unknown. In this study, we demonstrate for the first time that DcR3, a secreted decoy receptor that malignant pancreatic cancer cells express at a high level, acts as an extracellular antiapoptotic molecule by binding to TRAIL and counteracting its death-promoting function. The reduction of DcR3 with siRNA unmasked TRAIL and greatly enhanced TRAIL-induced apoptosis. Gemcitabine, a first-line drug for pancreatic cancer, also reduced the level of DcR3. The addition of DcR3 siRNA further enhanced gemcitabine-induced apoptosis. Notably, our in vivo study demonstrated that the therapeutic effect of gemcitabine could be enhanced via further reduction of DcR3, suggesting that downregulation of DcR3 in tumor cells could tip the balance of pancreatic cells towards apoptosis and potentially serve as a new strategy for pancreatic cancer therapy.
The interaction between Fe65 and Tip60 is regulated by S-nitrosylation on 440 cystein residue of Fe65  [PDF]
Eun Jeoung Lee, Sung Hwa Shin, Sunghee Hyun, Jaesun Chun, Sang Sun Kang
Advances in Biological Chemistry (ABC) , 2011, DOI: 10.4236/abc.2011.13013
Abstract: The S-Nitrosylation of protein thiol groups by NO is a widely recognized protein modification. The treat-ment of cells with NOBF4 induces the S-nitrosylation of FE65. In this study, we present evidence showing that FE65 modified by NO (Nitric Oxide) via S-nitrosylation induces functional changes in the protein that inhibits the HAT activity of Tip60. The results of mutational analysis of FE65 demonstrated further that the cysteine residue of FE65 (Cys440) is critical to the process of S-nitrosylation. The mutation of the cysteine residue which completely ablated the S-nitrosylation of FE65 also lost its inhibitory effects on Tip60 HAT activity. Thus, our findings show, for the first time, that the novel regulation mechanism of Tip60 activity may operate via FE65 binding, which is enhanced by S-nitrosylation on the FE65 Cys440 residue. This study describes the interaction between FE65 and Tip60, which is enhanced by a posttransla-tional modification of FE65 (through S-nitrosylation) by NO, promoting the association of the FE65-Tip60 protein complex and inhibiting both the HAT activity of Tip60 and cell death.
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