Design and assessment of short-in-length shape transition hypersonic inlet with circular throat

Changwon Lim,Sangwook Jin,박기수 대한기계학회 2023 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.37 No.11

This paper presents the design of an efficient, short-length shape transition inlet for hypersonic propulsion systems, operating at Mach 4 to 6. The inlet was shortened by approximately 24 % using a Busemann flow based on the median operating Mach number for streamline-tracing instead of the maximum operating Mach number. Additional upper circular arc of capture shape resulted in a compact compression surface that well preserves internal compression of the Busemann flow, and increased pressure rise by up to 31 % with higher total pressure recovery. The inlet was notched for maximum operating Mach number to minimize air spillage, and the range of operating Mach number and angle of attack was extended. Viscous effects were compensated by a proper truncation angle in order to maintain the exact circular throat shape for efficient manufacturing. The length-reduced inlet showed a wide operating range and high compression performance.

사거리 증대를 위한 이종추진제 덕티드 램제트 추진기관 궤적 성형

임창원(Changwon Lim),길현용(Hyunyong Gil) 항공우주시스템공학회 2023 항공우주시스템공학회 학술대회 발표집 Vol.2023 No.10

서로 다른 연소속도를 가지는 추진제를 적용하여 연료유량을 조절하는 고정노즐형 덕티드램제트 추진기관의 사거리 증대를 위한 사전 연구를 수행하였다. 현 설계영역에서는 빠르게 가속할 수 있는 높은 연료유량을 적용하여 높은 발사고각으로 발사할 수록 사거리가 증가하며, 흡입 공기유량이 적은 고고도에서는 연소효율을 높이기 위해 저속연소 추진제로 전환하는 것이 유리한 것으로 나타났다. 그러나 연료유량과 발사고각은 안정적인 흡입구 동작에 의해 제한되므로 적절한 마진을 확보하는 것이 필요하다.

Increased genetic susceptibility to intestinal‐type gastric cancer is associated with increased activity of the <i>RUNX</i>3 distal promoter

Lim, Byungho,Ju, Hyoungseok,Kim, Minjin,Kang, Changwon Wiley Subscription Services, Inc., A Wiley Company 2011 Cancer Vol.117 No.22

<P><B>Abstract</B></P><P><B>BACKGROUND:</B></P><P>The runt‐related transcription factor RUNX3 plays essential roles in various types of tumors, including gastric cancer. Epigenetic changes in the methylation of the <I>RUNX3</I> proximal promoter, but not common genetic changes in <I>RUNX3</I>, have been associated with both changes in the gene expression and development of the cancer.</P><P><B>METHODS:</B></P><P>A case‐control association study was conducted by genotyping 865 unrelated Korean subjects. Subsequent functional studies were performed to reveal functional implication of genetic association.</P><P><B>RESULTS:</B></P><P>Several single‐nucleotide polymorphisms (SNPs) in <I>RUNX3</I> were significantly associated with susceptibility to intestinal‐type gastric cancer (.0028 ≤ <I>P</I> ≤ .022) but not diffuse‐type gastric cancer (.70 ≤ <I>P</I> ≤ .96). The risk‐associated, minor variant of an intestinal‐type gastric cancer‐associated SNP in the <I>RUNX3</I> distal promoter (rs7528484) significantly increased promoter activity in a CREB1‐dependent manner. The distal promoter‐derived, 33 kDa isoform of RUNX3 increased the activity of transcription factor nuclear factor kappa B (NF‐κB), which had been activated by <I>Helicobacter pylori</I> infection, a risk factor for intestinal‐type gastric cancer, and the expression of the interleukin‐1β gene (<I>IL1B</I>), an NF‐κB target genetically and functionally associated with gastric cancer. In contrast, the proximal promoter‐derived, 44 kDa isoform of RUNX3 decreased both NF‐κB activity and <I>IL1B</I> expression.</P><P><B>CONCLUSIONS:</B></P><P>In addition to epigenetic changes in the <I>RUNX3</I> proximal promoter, genetic changes in the distal promoter may be associated with susceptibility to intestinal‐type gastric cancer by increasing promoter activity. Functionally, 2 RUNX3 isoforms may contribute differentially to intestinal‐type gastric cancer susceptibility, at least in part through regulating NF‐κB activity and <I>IL1B</I> expression Cancer 2011;. © 2011 American Cancer Society.</P>

Trichlorfon inhibits proliferation and promotes apoptosis of porcine trophectoderm and uterine luminal epithelial cells

Lim, Whasun,An, Yikyung,Yang, Changwon,Bazer, Fuller W.,Song, Gwonhwa Elsevier 2018 Environmental pollution Vol.242 No.1

<P><B>Abstract</B></P> <P>Trichlorfon is an organophosphate insecticide widely used in agriculture. Additionally, it is applied to pigs for control of endo- and ectoparasites. Previous studies have shown the effects of trichlorfon in pigs during late stages of gestation; however, little is known about its effects during early pregnancy, including implantation and placentation. We investigated whether trichlorfon affects proliferation and apoptosis of porcine trophectoderm (pTr) and uterine luminal epithelial (pLE) cells. Trichlorfon inhibited the proliferation of pTr and pLE cells, as evidenced by cell cycle arrest, and altered the expression of proliferation-related proteins. In addition, trichlorfon induced cell death and apoptotic features, such as loss of mitochondrial membrane potential and DNA fragmentation, in pTr and pLE cells. Moreover, trichlorfon treatment decreased concentrations of Ca<SUP>2+</SUP> in the cytoplasm in both cell lines and increased concentrations of Ca<SUP>2+</SUP> in mitochondria of pTr cells. Trichlorfon inhibited the activation of phosphoinositide 3-kinase/AKT and mitogen-activated protein kinase signaling pathways in pTr and pLE cells. Therefore, we suggest that trichlorfon-treated pTr and pLE cells exhibited abnormal cell physiology which might lead to early pregnancy failure.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Trichlorfon induces apoptosis and cell cycle arrest of porcine trophectoderm cells. </LI> <LI> Trichlorfon-induced oxidative stress results in mitochondrial membrane disruption. </LI> <LI> Trichlorfon inhibits the normal growth and survival of porcine trophoblast cells. </LI> <LI> Trichlorfon might lead to early pregnancy failure in pigs. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>A schematic diagram of mechanisms responsible for proapoptotic and antiproliferative effects of trichlorfon on pTr and pLE cells. Trichlorfon decreased the phosphorylation of PI3K/AKT and MAPK signaling proteins, which are normally activated during cell proliferation. Also, trichlorfon decreased the expression of PCNA and phosphorylation of cyclin D1 resulting in cell cycle arrest. In addition, a mitochondrial Ca<SUP>2+</SUP> overload induced by trichlorfon in pTr cells may be responsible for the decrease in mitochondrial membrane potential (MMP, Δψm). Loss of Δψm subsequently promoted apoptosis in pTr and pLE cells. Overall, exposure to trichlorfon decreased the viability of pTr and pLE cells which may cause pregnancy failure.</P> <P>[DISPLAY OMISSION]</P>

Quercetin Affects Spermatogenesis-Related Genes of Mouse Exposed to High-Cholesterol Diet

Changwon Yang,Hyocheol Bae,Gwonhwa Song,Whasun Lim 한국동물생명공학회(구 한국동물번식학회) 2020 Journal of Animal Reproduction and Biotechnology Vol.35 No.1

A high-cholesterol diet can reduce male fertility. However, it is not known whether a high-cholesterol diet can regulate the expression of genes involved in sperm maturation and sperm fertilizing ability. Quercetin, a natural product, is known to have cytoprotective effects by regulating lipid metabolism in various cell types. This study aimed to confirm the expression of genes involved in sperm maturation in the testes of mice fed a high-cholesterol diet and to determine whether quercetin can reverse the genetic regulation of cholesterol. Mice were divided into groups fed a normal chow diet and a high-cholesterol diet. Mice fed the high-cholesterol diet were dose-dependently supplemented with quercetin for 6 weeks. Investigations using quantitative PCR and in situ hybridization revealed that the high-cholesterol diet alters the expression of genes associated with sperm maturation in the testes of mice, and this was reversed with the supplementation of quercetin. In addition, the high-cholesterol diet regulated the expression of genes related to lipid metabolism in the liver of mice. Under a high-cholesterol diet, quercetin can improve male fertility by regulating the expression of genes involved in sperm maturation.

Luteolin Suppresses Proliferation of Choriocarcinoma Cells through Regulating PI3K/AKT Signaling Pathway and Blocking Transcriptional Activity of SREBP1

Changwon Yang,Whasun Lim,Gwonhwa Song 한국식품영양과학회 2016 한국식품영양과학회 학술대회발표집 Vol.2016 No.10

Coumestrol induces mitochondrial dysfunction by stimulating ROS production and calcium ion influx into mitochondria in human placental choriocarcinoma cells

Lim, Whasun,Yang, Changwon,Jeong, Muhah,Bazer, Fuller W,Song, Gwonhwa Oxford University Press 2017 Molecular human reproduction Vol.23 No.11

Palmitic acid induces inflammatory cytokines and regulates tRNA-derived stress-induced RNAs in human trophoblasts

Changwon Yang,Garam An,Jisoo Song,Gwonhwa Song,Whasun Lim The Korean Society of Animal Reproduction and Biot 2022 한국동물생명공학회지 Vol.37 No.4

High levels of proinflammatory cytokines have been observed in obese pregnancies. Obesity during pregnancy may increase the risk of various pregnancyrelated complications, with pathogenesis resulting from excessive inflammation. Palmitic acid (PA) is a saturated fatty acid that circulates in high levels in obese women. In our previous study, we found that PA inhibited the proliferation of trophoblasts developing into the placenta, induced apoptosis, and regulated the number of cleaved halves derived from transfer RNAs (tRNAs). However, it is not known how the expression of tRNA-derived stress-induced RNAs (tiRNAs) changes in response to PA treatment at concentrations that induce inflammation in human trophoblasts. We selected concentrations that did not affect cell viability after dose-dependent treatment of HTR8/SVneo cells, a human trophoblast cell line. PA (200 μM) did not affect the expression of apoptotic proteins in HTR8/SVneo cells. PA significantly increased the expression of inflammatory cytokines including interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α. In addition, 200 μM PA significantly increased the expression of tiRNAs compared to 800 μM PA treatment. These results suggest that PA impairs placental development during early pregnancy by inducing an inflammatory response in human trophoblasts. In addition, this study provides a basis for further research on the association between PA-induced inflammation and tiRNA generation.

<i>In</i> <i>silico</i> direct folding of thrombin-binding aptamer G-quadruplex at all-atom level

Yang, Changwon,Kulkarni, Mandar,Lim, Manho,Pak, Youngshang Oxford University Press 2017 Nucleic acids research Vol.45 No.22

<P><B>Abstract</B></P><P>The reversible folding of the thrombin-binding DNA aptamer G-quadruplexes (GQs) (TBA-15) starting from fully unfolded states was demonstrated using a prolonged time scale (10–12 μs) parallel tempering metadynamics (PTMetaD) simulation method in conjunction with a modified version of the AMBER bsc1 force field. For unbiased descriptions of the folding free energy landscape of TBA-15, this force field was minimally modified. From this direct folding simulation using the modified bsc1 force field, reasonably converged free energy landscapes were obtained in K<SUP>+</SUP>-rich aqueous solution (150 mM), providing detailed atomistic pictures of GQ folding mechanisms for TBA-15. This study found that the TBA folding occurred via multiple folding pathways with two major free energy barriers of 13 and 15 kcal/mol in the presence of several intermediate states of G-triplex variants. The early formation of these intermediates was associated with a single K<SUP>+</SUP> ion capturing. Interestingly, these intermediate states appear to undergo facile transitions among themselves through relatively small energy barriers.</P>

Homosalate aggravates the invasion of human trophoblast cells as well as regulates intracellular signaling pathways including PI3K/AKT and MAPK pathways

Yang, Changwon,Lim, Whasun,Bazer, Fuller W.,Song, Gwonhwa Elsevier 2018 Environmental pollution Vol.243 No.2

<P><B>Abstract</B></P> <P>Homosalate is an organic ultraviolet filter used in most sunscreens but has been reported to be toxic to marine organisms. The estrogenic activity of homosalate has also been reported, but its endocrine-disrupting effect remains unclear. Although homosalate has been detected in human placental tissues, its effect on the survival of human trophoblast cells needs to be investigated. Therefore, in this study, we evaluated if HTR8/SVneo, a human trophoblast cell line, treated with homosalate showed decreasing proliferative activity in a dose-dependent manner. Homosalate promoted the death of HTR8/SVneo cells with elevated lipid peroxidation and intracellular Ca<SUP>2+</SUP> concentration. It also induced endoplasmic reticulum stress and mitochondrial morphological disturbances associated with the differentiation of human trophoblast cells. However, when the intracellular Ca<SUP>2+</SUP> or reactive oxygen species were removed using BAPTA-AM or N-acetyl-L-cysteine (NAC), the cell proliferation suppressed by homosalate was restored. Homosalate also significantly inhibited the invasion of HTR8/SVneo cells. Furthermore, it modulated phosphoinositide 3-kinase (PI3K)/AKT and mitogen-activated protein kinase (MAPK) signaling pathways, which were involved in the cross-talk between both signaling pathways in HTR8/SVneo cells. Thus, homosalate adversely affects the survival, proliferation, and invasiveness of human trophoblast cells and therefore pregnant women should practice caution while using personal care products containing homosalate.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Homosalate inhibits survival and proliferation and invasion of human trophoblasts. </LI> <LI> Homosalate blocks AKT and MAPK signaling pathways in trophoblast cells. </LI> <LI> Homosalate-induced oxidative stress results in disruption of mitochondrial membrane. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>A schematic diagram illustrating current working hypothesis regarding the effects of homosalate on human trophoblast cells. Homosalate induces ROS production in human trophoblast cells, followed by excessive lipid peroxidation. Furthermore, elevated ROS increases cytosolic Ca<SUP>2+</SUP> concentration accompanied by loss of mitochondrial membrane potential (MMP). The disruption of mitochondrial membrane causes apoptotic cell death of human trophoblast cells. Moreover, homosalate activates phosphorylation of PI3K/AKT pathways and MAPK pathways with cross-talk between the two pathways. Finally, the alteration of signaling pathways causes transcriptional regulation in nucleus, leading to downregulation of proliferation and invasion of human trophoblast cells.</P> <P>[DISPLAY OMISSION]</P>