Planar Spiral Coil Design for a Pulsed Induction Metal Detector to Improve the Sensitivities

Bobae Kim,Seung-hoon Han,Kangwook Kim IEEE 2014 IEEE antennas and wireless propagation letters Vol.13 No.-

<P>In a pulsed induction metal detector system, the sensitivity variation for detectable minimum metal target and the maximum detection distance are investigated as the winding geometry of the search coil is varied. A number of planar square spiral mono coils with various fill ratios and wire spacing-to-width ratios are comparatively analyzed based on a numerical simulation. Five representative coils are fabricated and applied to a pulsed induction metal detector system as a search coil. It is demonstrated that a search coil with a larger fill ratio has a high size sensitivity for a minimum metal target at close distances, which may be missed by coils with smaller fill ratios. A search coil with a smaller wire spacing-to-width ratio is shown to have a high depth sensitivity for maximum detection distances.</P>

Pulse-induction metal detector with time-domain bucking circuit for landmine detection

Bobae Kim,Jung Won Yoon,Seung-eui Lee,Seung-Hoon Han,Kangwook Kim IET 2015 Electronics letters Vol.51 No.2

<P>A novel pulse-induction (PI) metal detector (MD) is proposed to decrease the saturation time of the output voltage and increase the detection depth. The proposed MD utilises a receiver with a time-domain bucking circuit. The bucking circuit decreases the output voltage significantly without a target, so that the output voltage can be amplified more before becoming saturated. To demonstrate the performance of the proposed MD, it has been fabricated and measured. The measured output voltage shows that the saturation time is reduced and that the detection depth increases in comparison with a conventional PI MD.</P>

mGluR2/3 in the Lateral Amygdala is Required for Fear Extinction: Cortical Input Synapses onto the Lateral Amygdala as a Target Site of the mGluR2/3 Action

Kim, Jihye,An, Bobae,Kim, Jeongyeon,Park, Sewon,Park, Sungmo,Hong, Ingie,Lee, Sukwon,Park, Kyungjoon,Choi, Sukwoo American College of Neuropsychopharmacology 2015 Neuropsychopharmacology Vol.40 No.13

Various subtypes of metabotropic glutamate receptors (mGluRs) have been implicated in fear extinction, but mGluR2/3 subtype has not been tested. Here, we found that microinjection of an mGluR2/3 antagonist, LY341495, into the lateral amygdala (LA), but not into the adjacent central amygdala (CeA), impaired extinction retention without affecting within-session extinction. In contrast, we failed to detect any significant changes in motility and anxiety during a period when extinction training or retention was performed after LY341495 injection, suggesting that the effect of LY341495 is specific to conditioned responses. Subsequently, on the basis of a previous finding that a long-term potentiation of presynaptic efficacy at cortical input synapses onto the lateral amygdala (C-LA synapses) supports conditioned fear, we tested the hypothesis that activation of mGluR2/3 leads to fear extinction via a long-term weakening of presynaptic functions at C-LA synapses. Fear extinction produced a decrease in C-LA synaptic efficacy, whereas LY341495 infusion into the LA blocked this extinction-induced C-LA efficacy decrease without altering synaptic efficacy at other LA synapses. Furthermore, extinction enhanced paired pulse ratio (PPR) of EPSCs, which inversely correlates with presynaptic release probability, whereas LY341495 infusion into the LA attenuated the extinction-induced increase in PPR, suggesting the presence of mGluR2/3-dependent presynaptic changes after extinction. Consistently, extinction occluded a presynaptic form of depression at C-LA synapses, whereas the LY341495 infusion into the LA rescued this occlusion. Together, our findings suggest that mGluR2/3 is required for extinction retention and that the mGluR2/3 action is mediated by the long-term weakening of release probability at C-LA synapses.

Bandwidth Enhancement for SSN Suppression Using a Spiral-Shaped Power Island and a Modified EBG Structure for a λ/4 Open Stub

Bobae Kim,Dong-Wook Kim 한국전자통신연구원 2009 ETRI Journal Vol.31 No.2

This paper proposes a spiral-shaped power island structure that can effectively suppress simultaneous switching noise (SSN) when the power plane drives high-speed integrated circuits in a small area. In addition, a new technique is presented which greatly improves the resonance peaks in a stopband by utilizing λ/4 open stubs on a conventional periodic electromagnetic bandgap (EBG) power plane. Both proposed structures are simulated numerically and experimentally verified using commercially available 3D electromagnetic field simulation software. The results demonstrate that they achieve better SSN suppression performance than conventional periodic EBG structures.

Mutation in the DNA-binding domain of the EWS-Oct-4 oncogene results in dominant negative activity that interferes with EWS-Oct-4-mediated transactivation

Kim, Sol,Lee, Jungwoon,Kim, Ja Young,Lim, Bobae,Shin, Eung-Kyun,Han, Yong-Mahn,Kim, Sung-Su,Song, Jin-Ho,Kim, Jungho Wiley Subscription Services, Inc., A Wiley Company 2009 International journal of cancer: Journal internati Vol.124 No.10

<P>The EWS-Oct-4 protein is a chimeric molecule in which the amino terminal domain (NTD) of the EWS becomes fused to the carboxy terminal domain (CTD) of the Oct-4 transcription factor. It was identified in human bone and soft-tissue tumors associated with t(6;22)(p21;q12). Using in vitro and in vivo systems, we found that the EWS-Oct-4 protein self-associates. The major domains required for self-association mapped to the EWS NTD (amino acids 70–163) and the POU DNA-binding domain. EWS-Oct-4 protein also associated with EWS-Oct-4 (V351P), which contains a mutation in the POU DNA-binding domain. Using electrophoretic mobility shift assays, we found that the EWS-Oct-4 (V351P) mutant interfered with wild-type EWS-Oct-4 DNA-binding activity. In addition, we found that EWS-Oct-4-mediated transcriptional activation was inhibited by EWS-Oct-4 (V351P) protein in vivo. Thus, this mutation in the POU DNA-binding domain results in a dominant negative protein. These findings suggest that the biological functions of the EWS-Oct-4 oncogene can be modulated by the dominant negative mutant EWS-Oct-4 (V351P). © 2008 Wiley-Liss, Inc.</P>

Syringin attenuates insulin resistance via adiponectin-mediated suppression of low-grade chronic inflammation and ER stress in high-fat diet-fed mice

Kim, Bobae,Kim, Min-Seok,Hyun, Chang-Kee Academic Press 2017 Biochemical and biophysical research communication Vol. No.

<P><B>Abstract</B></P> <P>In the treatment of type 2 diabetes, improvements in glucose control are often linked to side effects such as weight gain and altered lipid metabolism, increasing the risk of cardiovascular disease. It is therefore important to develop antidiabetic drugs that exert beneficial effects on insulin sensitivity and lipid metabolism at the same time. Here we demonstrate that syringin, a naturally occurring glucoside, improves glucose tolerance without increased weight gain in high-fat diet-induced obese mice. Syringin augmented insulin-stimulated Akt phosphorylation in skeletal muscle, epididymal adipose tissue (EAT), and the liver, showing an insulin-sensitizing activity. Syringin-treated mice also showed markedly elevated adiponectin production in EAT and suppressed expression of pro-inflammatory cytokines in peripheral tissues, indicating a significant reduction in low-grade chronic inflammation. Additionally, syringin enhanced AMP-activated protein kinase activity and decreased the expression of lipogenic genes in skeletal muscle, which was associated with reduced endoplasmic reticulum (ER) stress. Taken together, our data suggest that syringin attenuates HFD-induced insulin resistance through the suppressive effect of adiponectin on low-grade inflammation, lipotoxicity, and ER stress, and show syringin as a potential therapeutic agent for prevention and treatment of type 2 diabetes with low risk of adverse effects such as weight gain and dysregulated lipid metabolism.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Syringin enhances insulin sensitivity under HF feeding condition. </LI> <LI> Akt phosphorylation was increased in skeletal muscle, EAT, and the liver. </LI> <LI> Adiponectin-mediated AMPK activation in skeletal muscle was augmented. </LI> <LI> Pro-inflammatory cytokine expression was reduced in muscle, EAT, and the liver. </LI> <LI> Expression of genes related to ER stress was reduced in skeletal muscle. </LI> </UL> </P>

Immunomodulatory Effects of Dioscoreae Rhizome Against Inflammation through Suppressed Production of Cytokines Via Inhibition of the NF-${\kappa}B$ Pathway

Kim, Seulah,Shin, Seulmee,Hyun, Bobae,Kong, Hyunseok,Han, Shinha,Lee, Aeri,Lee, Seungjeong,Kim, Kyungjae The Korean Association of Immunobiologists 2012 Immune Network Vol.12 No.5

Dioscoreae Rhizome (DR) has been used in traditional medicine to treat numerous diseases and is reported to have anti-diabetes and anti-tumor activities. To identify a bioactive traditional medicine with anti-inflammatory activity of a water extract of DR (EDR), we determined the mRNA and protein levels of proinflammatory cytokines in macrophages through RT-PCR and western blot analysis and performed a FACS analysis for measuring surface molecules. EDR dose-dependently decreased the production of NO and pro-inflammatory cytokines such as IL-$1{\beta}$, IL-6, TNF-${\alpha}$, and $PGE_2$, as well as mRNA levels of iNOS, COX-2, and pro-inflammatory cytokines, as determined by western blot and RT-PCR analysis, respectively. The expression of co-stimulatory molecules such as B7-1 and B7-2 was also reduced by EDR. Furthermore, activation of the nuclear transcription factor, NF-${\kappa}B$, but not that of IL-4 and IL-10, in macrophages was inhibited by EDR. These results show that EDR decreased pro-inflammatory cytokines via inhibition of NF-${\kappa}B$-dependent inflammatory protein level, suggesting that EDR could be a useful immunomodulatory agent for treating immunological diseases.

A Dual-Mode Power Amplifier With On-Chip Switch Bias Control Circuits for LTE Handsets

Bobae Kim,Cholho Kwak,Jongsoo Lee IEEE 2011 IEEE TRANSACTIONS ON CIRCUITS AND SYSTEMS PART 2 E Vol.58 No.12

<P>In this brief, we present a dual-mode (high and low) power amplifier (PA) for fourth-generation long-term evolution (LTE) handset applications using a device switching technique to improve the efficiency at low output power. In particular, the effects of the gate voltage variation of the input and output switches on the amplifier performances are described. In addition, a bias control circuit for a dual-mode PA, which can provide the correct voltage to the input and output switches and can be effectively controlled by the mode control voltage, is also proposed. The bias control circuit, the mode switch, and the PA are implemented with the integrated pseudomorphic high-electron mobility transistor (pHEMT) and heterojunction bipolar transistor (HBT) technology on the same chip (i.e., bipolar field effect transistor process). A dual-mode PA with a gain of 27.2 dB, PAE of 34.5%, a ACLR<SUB>E-UTRA</SUB> value of -31.2 dBc, and error vector magnitude (EVM) of 2.97% has been achieved in high-power mode; whereas a 22 dB of gain, PAE of 19%, a ACLR<SUB>E-UTRA</SUB> value of -31.6 dBc and EVM of 2.84% were measured in the low-power mode with LTE uplink signals.</P>

CCCTC-binding factor is essential to the maintenance and quiescence of hematopoietic stem cells in mice

Kim, Tae-Gyun,Kim, Sueun,Jung, Soyeon,Kim, Mikyoung,Yang, Bobae,Lee, Min-Geol,Kim, Hyoung-Pyo Nature Publishing Group 2017 Experimental and molecular medicine Vol.49 No.8

<P>Hematopoiesis involves a series of lineage differentiation programs initiated in hematopoietic stem cells (HSCs) found in bone marrow (BM). To ensure lifelong hematopoiesis, various molecular mechanisms are needed to maintain the HSC pool. CCCTC-binding factor (CTCF) is a DNA-binding, zinc-finger protein that regulates the expression of its target gene by organizing higher order chromatin structures. Currently, the role of CTCF in controlling HSC homeostasis is unknown. Using a tamoxifen-inducible CTCF conditional knockout mouse system, we aimed to determine whether CTCF regulates the homeostatic maintenance of HSCs. In adult mice, acute systemic CTCF ablation led to severe BM failure and the rapid shrinkage of multiple c-Kit<SUP>hi</SUP> progenitor populations, including Sca-1<SUP>+</SUP> HSCs. Similarly, hematopoietic system-confined CTCF depletion caused an acute loss of HSCs and highly increased mortality. Mixed BM chimeras reconstituted with supporting BM demonstrated that CTCF deficiency-mediated HSC depletion has both cell-extrinsic and cell-intrinsic effects. Although c-Kit<SUP>hi</SUP> myeloid progenitor cell populations were severely reduced after ablating <I>Ctcf</I>, c-Kit<SUP>int</SUP> common lymphoid progenitors and their progenies were less affected by the lack of CTCF. Whole-transcriptome microarray and cell cycle analyses indicated that CTCF deficiency results in the enhanced expression of the cell cycle-promoting program, and that CTCF-depleted HSCs express higher levels of reactive oxygen species (ROS). Importantly, <I>in vivo</I> treatment with an antioxidant partially rescued c-Kit<SUP>hi</SUP> cell populations and their quiescence. Altogether, our results suggest that CTCF is indispensable for maintaining adult HSC pools, likely by regulating ROS-dependent HSC quiescence.</P>

Performance Measurement of a Photodiode Sensor Coupled with a Scintillator

Kim, Bobae,Kang, Kookhyun,Kim, Taehun,Kim, Hongjoo,Park, Hwanbae,Lee, Seungchul,Jeon, Hyebin Korean Physical Society 2016 New Physics: Sae Mulli Vol.66 No.3