Student Recital: Myung-Hee Chung, Piano; May 1, 1975

Centennial East Recital HallThursday EveningMay 1, 19758:15 p.m

Student Recital: Myung-Hee Chung, Piano; February 24, 1976

Recital HallTuesday EveningFebruary 24, 19768:15 p.m

Student Trio Recital: Ricardo Mariani, Clarinet; Myung Hee Chung, Piano; Tom Wang, Cello; November 19, 1975

Hayden AuditoriumWednesday EveningNovember 19, 19758:15 p.m

Investigation of Enhanced Polygon Wall Boundary Model in PNU-MPS Method

With regard to demonstration of fluid flow, there are two descriptions which are Eulerian description and Lagrangian description. In the field of CFD (Computational Fluid Dynamics), a number of studies relevant to grid method based on Eulerian description have been conducted generally. However, when the grid method is employed to simulate flow field, it is inevitable to give consideration to convection term which generates severe numerical diffusion and fluctuation. To obtain the accuracy of solution, a different type of method based on Lagrangian description is come to the fore. Numerical approaches following Lagrangian description have been called meshfree or particle method. Even though particle method does not accompany convection term and fully satisfies conservation of mass, its studies have not been carried out extensively because it is difficult to implement the boundary conditions correctly due to insufficient number of particles in the vicinity of boundary. It affects directly the stability of flow field and accuracy in computation. In MPS (Moving Particle Semi-implicit) method [1], fixed-type of dummy particles are placed inside wall boundary. By placing extra particles as the wall, it seems to be not easy to satisfy the boundary condition for sharp-edged or extremely thin body configuration. In this study, the enhanced polygon wall boundary model, which was suggested originally by Mitsume et al. [2], is employed to the PNU-MPS (Pusan-National-University-modified MPS) method [3] to improve and stabilize the analysis of fluid flow with arbitrary-shaped body including sharp-edged body configuration without any additional particles. The developed simulation method, called as PNU-MPS-POLY, is adopted to the Couette flow and the lid-driven cavity flow with various corner angles. The present simulation results are validated through comparison with the analytic solutions, the experiments [4], and other simulation results [5,6]

Proteomic and biochemical analyses reveal the activation of unfolded protein response, ERK-1/2 and ribosomal protein S6 signaling in experimental autoimmune myocarditis rat model

<p>Abstract</p> <p>Background</p> <p>To investigate the molecular and cellular pathogenesis underlying myocarditis, we used an experimental autoimmune myocarditis (EAM)-induced heart failure rat model that represents T cell mediated postinflammatory heart disorders.</p> <p>Results</p> <p>By performing unbiased 2-dimensional electrophoresis of protein extracts from control rat heart tissues and EAM rat heart tissues, followed by nano-HPLC-ESI-QIT-MS, 67 proteins were identified from 71 spots that exhibited significantly altered expression levels. The majority of up-regulated proteins were confidently associated with unfolded protein responses (UPR), while the majority of down-regulated proteins were involved with the generation of precursor metabolites and energy metabolism in mitochondria. Although there was no difference in AKT signaling between EAM rat heart tissues and control rat heart tissues, the amounts and activities of extracellular signal-regulated kinase (ERK)-1/2 and ribosomal protein S6 (rpS6) were significantly increased. By comparing our data with the previously reported myocardial proteome of the Coxsackie viruses of group B (CVB)-mediated myocarditis model, we found that UPR-related proteins were commonly up-regulated in two murine myocarditis models. Even though only two out of 29 down-regulated proteins in EAM rat heart tissues were also dysregulated in CVB-infected rat heart tissues, other proteins known to be involved with the generation of precursor metabolites and energy metabolism in mitochondria were also dysregulated in CVB-mediated myocarditis rat heart tissues, suggesting that impairment of mitochondrial functions may be a common underlying mechanism of the two murine myocarditis models.</p> <p>Conclusions</p> <p>UPR, ERK-1/2 and S6RP signaling were activated in both EAM- and CVB-induced myocarditis murine models. Thus, the conserved components of signaling pathways in two murine models of acute myocarditis could be targets for developing new therapeutic drugs or methods aimed at treating enigmatic myocarditis.</p

Early postictal electroencephalography and correlation with clinical findings in children with febrile seizures

PurposeElectroencephalography (EEG) is frequently ordered for patients with febrile seizures despite its unclear diagnostic value. We evaluated the prevalence of abnormal EEGs, the association between clinical findings and abnormal EEGs, and the predictive value of EEG for the recurrence of febrile seizures.MethodsData were collected on 230 children who were treated for febrile seizures at Kyung Hee University Medical Center from 2005 to 2009. EEGs were recorded after 1-2 days of hospitalization when children became afebrile. EEG patterns were categorized as normal, epileptiform, or nonspecific relative to abnormalities. The patients' medical records were reviewed, and telephone interviews with the families of the children were conducted to inquire about seizure recurrence. The relationships between clinical variables, including seizure recurrence, and EEG abnormalities were evaluated.ResultsOf the 131 children included, 103 had simple and 28 had complex febrile seizures. EEG abnormalities were found in 41 children (31%). EEG abnormalities were more common in children with complex than simple febrile seizures (43% vs. 28%), but the difference was not statistically significant. Logistical regression analysis showed that having multiple seizures in a 24-hour period was significantly predictive of abnormal EEG (odds ratio, 2.98; 95% confidence interval, 1.0 to 88; P=0.048). The frequency of recurrence did not differ significantly in the normal (31%) and abnormal (23%) EEG groups.ConclusionMultiple seizures within 24 hours were predictive of abnormal EEG in children with febrile seizures. Abnormal EEG was not predictive of febrile seizure recurrence

Exogenous 8-hydroxydeoxyguanosine attenuates doxorubicin-induced cardiotoxicity by decreasing pyroptosis in H9c2 cardiomyocytes

Doxorubicin (DOX), which is widely used in cancer treatment, can induce cardiomyopathy. One of the main mechanisms whereby DOX induces cardiotoxicity involves pyroptosis through the NLR family pyrin domain containing 3 (NLRP3) inflammasome and gasdermin D (GSDMD). Increased NAPDH oxidase (NOX) and oxidative stress trigger pyroptosis. Exogenous 8-hydroxydeoxyguanosine (8-OHdG) decreases reactive oxygen species (ROS) production by inactivating NOX. Here, we examined whether 8-OHdG treatment can attenuate DOX-induced pyroptosis in H9c2 cardiomyocytes. Exposure to DOX increased the peroxidative glutathione redox status and NOX1/2/4, toll-like receptor (TLR)2/4, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) expression, while an additional 8-OHdG treatment attenuated these effects. Furthermore, DOX induced higher expression of NLRP3 inflammasome components, including NLRP3, apoptosis-associated speck-like protein containing a c-terminal caspase recruitment domain (ASC), and pro-caspase-1. Moreover, it increased caspase-1 activity, a marker of pyroptosis, and interleukin (IL)-1β expression. All these effects were attenuated by 8-OHdG treatment. In addition, the expression of the cardiotoxicity markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was increased by DOX, whereas the increase of ANP and BNP induced by DOX treatment was reversed by 8-OHdG. In conclusion, exogenous 8-OHdG attenuated DOX-induced pyroptosis by decreasing the expression of NOX1/2/3, TLR2/4, and NF-κB. Thus, 8-OHdG may attenuate DOX-induced cardiotoxicity through the inhibition of pyroptosis.This research was funded by a grant from the National Research Foundation of Korea (NRF) grant (2020R1A2C200652811) (to K.H.S.) and Korea Environment Industry & Technology Institute (KEITI) through ‑Core Technology Development Project for Environmental Diseases Prevention and Management Program, funded by Korea Ministry of Environment (MOE) (2021003310006) (to K.H.S.