• Korean Journal of Community Nutrition
• /
• v.16 no.1
• /
• pp.126-135
• /
• 2011

Obesity is characterized by increased storage of fatty acids in an adipose tissue and closely associated with the development of insulin resistance and cardiovascular diseases (CVD) through secretion of adipokines. This study was done to compare serum insulin, leptin, adiponectin and high sensitivity C-reactive protein (hs-CRP) levels according to body masss index (BMI) in Korean adult women aged 19 to 50. In addition, we examined the association of BMI, serum lipids and Homa-IR with serum adiponectin, leptin and hs-CRP levels. The subjects were divided into 3 groups by their BMI, normal weight (BMI ${\leq}$ 22.9, n = 30), overweight (23.0 ${\leq}$ BMI ${\leq}$ 24.9, n = 71) and obese group (25.0 ${\leq}$ BMI, n = 59). Serum levels of total-cholesterol, TG, and LDL-cholesterol were significantly higher in obese group than in normal weight group. LDL/HDL ratio and AI were significantly higher in obese group than in normal or overweight group. Fasting serum levels of glucose and insulin and Homa-IR as a marker of insulin resistance were significantly higher in obese group than in overweight group. Serum leptin level was significantly higher in obese group while serum adiponectin level was significantly lower in obese group compared to other two groups. hs-CRP was significantly increased in obese group. Correlation data show that serum adiponectin level was positively correlated with serum HDLcholesterol level and was negatively correlated with BMI, WC, TG, LDL-cholesterol, Homa-IR, hs-CRP and leptin. In addition, serum leptin level was positively correlated with BMI, WC, glucose, insulin, Homa-IR and hs-CRP. These results might imply that the regulation of key adipokines such as adiponectin might be a strategy for the prevention or treatment of obesity-associated diseases such as diabetes and CVD.

• Journal of the Korea Society of Computer and Information
• /
• v.13 no.5
• /
• pp.187-193
• /
• 2008

Interface technologies for a user to control home automation system in wearable computing environment has been studied recently. This paper proposes a new interface method for a disabled person to control home automation system in wearable computing environment by using EOG sensing circuit and marker recognition. In the proposed interface method, the operations of a home network device are represented with human readable markers and displayed around the device. A user wearing a HMD, a video camera, and a computer selects the desired operation by seeing the markers and selecting one of them with eye movement from the HMD display The requested operation is executed by sending the control command for the selected marker to the home network control device. By using the EOG sensing circuit and the marker recognition system a user having problem with moving hands and fit can manipulate a home automation system with only eye movement.

• Journal of Preventive Medicine and Public Health
• /
• v.45 no.2
• /
• pp.62-69
• /
• 2012

Objectives: Chronic inflammation is now thought to play a key pathogenetic role in the associations of obesity with insulin resistance and diabetes. Based on our recent findings on persistent organic pollutants (POPs) including the lack of an association between obesity and either insulin resistance or diabetes prevalence among subjects with very low concentrations of POPs, we hypothesized that POP concentrations may be associated with inflammation and modify the associations between inflammation and insulin resistance in non-diabetic subjects. Methods: Cross-sectional associations among serum POPs, C-reactive protein (CRP), and homeostasis model assessment of insulin resistance (HOMA-IR) were investigated in 748 non-diabetic participants aged ${\geq}20$ years. Nineteen types of POPs in 5 subclasses were selected because the POPs were detectable in ${\geq}60%$ of the participants. Results: Among the five subclasses of POPs, only organochlorine (OC) pesticides showed positive associations with CRP concentrations, while polychlorinated biphenyls (PCBs) showed inverse associations with CRP concentrations. There were statistically significant interactions between CRP and OC pesticides and between CRP and PCBs, in estimating HOMA-IR (P for interaction <0.01 and <0.01, respectively). CRP was not associated with HOMA-IR among subjects with low concentrations of OC pesticides or PCBs, while CRP was strongly associated with HOMA-IR among subjects with high concentrations of these POPs. Conclusions: In the current study, OC pesticides were associated with increased levels of CRP, a marker of inflammation, and both OC pesticides and PCBs may also modify the associations between CRP and insulin resistance.

• Journal of Radiation Protection and Research
• /
• v.34 no.2
• /
• pp.49-54
• /
• 2009

Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging and also contributes to their unfavorable effects in cultured cells and animal tissues. This study was conducted to investigate the effect of ionizing radiation (IR) on mtDNA deletion and the involvement of reactive oxygen species (ROS) in this process in human lung fibroblast (IMR-90) cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated with $^{137}Cs$ $\gamma$-rays and the intracellular ROS level was determined by 2',7'-dichlorofluorescein diacetate (DCFH-DA) and mtDNA common deletion (4977bp) was detected by nested PCR. Old cells at PD 55 and $H_2O_2$-treated young cells were compared as the positive control. IR increased the intracellular ROS level and mtDNA 4977 bp deletion in IMR-90 cells dose-dependently. The increases of ROS level and mtDNA deletion were also observed in old cells and $H_2O_2$-treated young cells. To confirm the increased ROS level is essential for mtDNA deletion in irradiated cells, the effects of N-acetylcysteine (NAC) on IRinduced ROS and mtDNA deletion were examined. 5 mM NAC significantly attenuated the IR-induced ROS increase and mtDNA deletion. These results suggest that IR induces the mtDNA deletion and this process is mediated by ROS in IMR-90 cells.

• Journal of Radiation Protection and Research
• /
• v.36 no.3
• /
• pp.119-126
• /
• 2011

Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging, and contributes to harmful effects in cultured cells and animal tissues. mtDNA biogenesis genes (NRF-1, TFAM) are essential for the maintenance of mtDNA, as well as the transcription and replication of mitochondrial genomes. Considering that oxidative stress is known to affect mitochondrial biogenesis, we hypothesized that ionizing radiation (IR)-induced reactive oxygen species (ROS) causes mtDNA deletion by modulating the mitochondrial biogenesis, thereby leading to cellular senescence. Therefore, we examined the effects of IR on ROS levels, cellular senescence, mitochondrial biogenesis, and mtDNA deletion in IMR-90 human lung fibroblast cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated at 4 or 8 Gy. Old cells at PD55, and H2O2-treated young cells at PD 39, were compared as a positive control. The IR increased the intracellular ROS level, senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) activity, and mtDNA common deletion (4977 bp), and it decreased the mRNA expression of NRF-1 and TFAM in IMR-90 cells. Similar results were also observed in old cells (PD 55) and $H_2O_2$-treated young cells. To confirm that a increase in ROS level is essential for mtDNA deletion and changes of mitochondrial biogenesis in irradiated cells, the effects of N-acetylcysteine (NAC) were examined. In irradiated and $H_2O_2$-treated cells, 5 mM NAC significantly attenuated the increases of ROS, mtDNA deletion, and SA-${\beta}$-gal activity, and recovered from decreased expressions of NRF-1 and TFAM mRNA. These results suggest that ROS is a key cause of IR-induced mtDNA deletion, and the suppression of the mitochondrial biogenesis gene may mediate this process.

• Journal of Institute of Control, Robotics and Systems
• /
• v.12 no.11
• /
• pp.1074-1080
• /
• 2006

Motion capture systems are gaining popularity in entertainment, medicine, sports, education, and industry, with animation and gaming applications for entertainment taking the lead. A wide variety of systems are available for motion capture, but most of them are complicated and expensive. In the general class of optical motion capture, two or more optical sensors are needed to measure the 3D positions of the markers attached to the body. Recently, a 3D motion capture system using two Position Sensitive Detector (PSD) optical sensors was introduced to capture high-speed motion of an active infrared LED marker. The PSD-based system, however, is limited by a geometric calibration procedure for two PSD sensor modules that is too difficult for common customers. In this research, we have introduced a new system that used a single PSD sensor unit to obtain 3D positions of active IR LED-based markers. This new system is easy to calibrate and inexpensive.

• Proceedings of the KIEE Conference
• /
• 2008.10b
• /
• pp.379-381
• /
• 2008

본 논문에서는 가정용 비디오 게임에 사용 가능한 고속의 저가형 모션캡쳐, 시스템에 사용되는 전 방향 특성을 갖는 IR 능동 마커의 개발을 목표로 하고 있다. 현재 영화나 게임에서 모션캡쳐를 응용한 시스템 및 컨텐츠들이 많이 선보기고 있으며, 인기를 모으고 있는 추세이다. 이러한 흐름에 맞추어 우리는 이미 저가이면서 속도가 빠른 PSD(Position Sensitive Detector) 센서를 이용만 스테레오 비젼 기반의 PSD 모션캡쳐 시스템(Stereo vision based PSD motion capture system)과 광량 보정 기반의 단일 PSD 모션캡쳐 시스템(Intensity Calibration based single PSD motion capture system) 그리고 일정간격의 두 능동마커 기반의 단안 PSD 모션캡쳐 시스템(Two active markers at fixed distance based single PSD motion capture system)등을 소개한 바 있다. 본 논문에서 제안하는 전방향 특성을 갖는 IR 능동 마커는 일정간격의 두 능동마커 기반의 단안 PSD 모션캡쳐 시스템에 적용하여 보다 정밀한 3차원 좌표 측정을 할 수 있도록 한다. 이를 위해 본 논문에서는 동일 특성을 갖는 마커를 제작하고 평가하여 일정간격의 두 능동마커 기반의 단안 PSD 모션캡쳐 시스템에 적합한 마커의 제작 방법을 제안하였다.

• Journal of Korean Neurosurgical Society
• /
• v.56 no.6
• /
• pp.488-491
• /
• 2014

Objective : The purpose of this study was to investigate the prenatal hypoxic effect on the fetal brain development. Methods : We used the guinea pig chronic placental insufficiency model to investigate the effect of hypoxia on fetal brain development. We ligated unilateral uterine artery at 30-32 days of gestation (dg : with term defined as -67 dg). At 50 dg, 60 dg, fetuses were sacrificed and assigned to either the growth-restricted (GR) or control (no ligation) group. After fixation, dissection, and sectioning of cerebral tissue from these animals, immunohistochemistry was performed with NeuN antibody, which is a mature neuronal marker in the cerebral cortex. Results : The number of NeuN-immunoreactive (IR) cells in the cerebral cortex did not differ between the GR and control groups at 50 dg. However, the number of NeuN-IR cells was lesser in GR fetuses than in controls at 60 dg (p<0.05). Conclusion : These findings show that chronic prenatal hypoxia affect the number of neuron in the cerebral cortex of guinea pig fetus at 60 dg. The approach used in this study is helpful for extending our understanding of neurogenesis in the cerebral cortex, and the findings may be useful for elucidating the brain injury caused by prenatal hypoxia.

• Journal of Plant Biotechnology
• /
• v.46 no.4
• /
• pp.323-330
• /
• 2019

The high expression level of industrial and metabolically important proteins in plants can be achieved by plastid transformation. The CaIA vector, a Capsicum-specific vector harboring aadA (spectinomycin resistance), is a selectable marker controlled by the PsbA promoter, and the terminator is flanked by the trnA and trnI regions of the inverted repeat (IR) region of the plastid. The CaIA vector can introduce foreign genes into the IR region of the plastid genome. The biolistic method was used for chloroplast transformation in Scoparia dulcis with leaf explants followed by antibiotic selection on regeneration medium. Transplastomes were successfully screened, and the transformation efficiency of 3 transgenic lines from 25 bombarded leaf explants was determined. Transplastomic lines were evaluated by PCR and Southern blotting for the confirmation of aadA insertion and its integration into the chloroplast genome. Seeds collected from transplastomes were analyzed on spectinomycin medium with wild types to determine genetic stability. The increased chloroplast transformation efficiency (3 transplastomic lines from 25 bombarded explants) would be useful for expressing therapeutically and industrially important genes in Scoparia dulcis L.

• The Korean Journal of Physiology and Pharmacology
• /
• v.22 no.6
• /
• pp.661-670
• /
• 2018

Fimasartan, a new angiotensin II receptor antagonist, reduces myocyte damage and stabilizes atherosclerotic plaque through its anti-inflammatory effect in animal studies. We investigated the protective effects of pretreatment with fimasartan on ischemia-reperfusion injury (IRI) in a mouse model of ischemic renal damage. C57BL/6 mice were pretreated with or without 5 (IR-F5) or 10 (IR-F10) mg/kg/day fimasartan for 3 days. Renal ischemia was induced by clamping bilateral renal vascular pedicles for 30 min. Histology, pro-inflammatory cytokines, and apoptosis assays were evaluated 24 h after IRI. Compared to the untreated group, blood urea nitrogen and serum creatinine levels were significantly lower in the IR-F10 group. IR-F10 kidneys showed less tubular necrosis and interstitial fibrosis than untreated kidneys. The expression of F4/80, a macrophage infiltration marker, and tumor necrosis factor $(TNF)-{\alpha}$, decreased in the IR-F10 group. High-dose fimasartan treatment attenuated the upregulation of $TNF-{\alpha}$, interleukin $(IL)-1{\beta}$, and IL-6 in ischemic kidneys. Fewer TUNEL positive cells were observed in IR-F10 compared to control mice. Fimasartan caused a significant decrease in caspase-3 activity and the level of Bax, and increased the Bcl-2 level. Fimasartan preserved renal function and tubular architecture from IRI in a mouse ischemic renal injury model. Fimasartan also attenuated upregulation of inflammatory cytokines and decreased apoptosis of renal tubular cells. Our results suggest that fimasartan inhibited the process of tubular injury by preventing apoptosis induced by the inflammatory pathway.