• Integrative Medicine Research
• /
• v.2 no.4
• /
• pp.131-138
• /
• 2013

The skeletal muscle in our body is a major site for bioenergetics and metabolism during exercise. Carbohydrates and fats are the primary nutrients that provide the necessary energy required to maintain cellular activities during exercise. The metabolic responses to exercise in glucose and lipid regulation depend on the intensity and duration of exercise. Because of the increasing prevalence of obesity, recent studies have focused on the cellular and molecular mechanisms of obesity-induced insulin resistance in skeletal muscle. Accumulation of intramyocellular lipid may lead to insulin resistance in skeletal muscle. In addition, lipid intermediates (e.g., fatty acyl-coenzyme A, diacylglycerol, and ceramide) impair insulin signaling in skeletal muscle. Recently, emerging evidence linking obesity-induced insulin resistance to excessive lipid oxidation, mitochondrial overload, and mitochondrial oxidative stress have been provided with mitochondrial function. This review will provide a brief comprehensive summary on exercise and skeletal muscle metabolism, and discuss the potential mechanisms of obesity-induced insulin resistance in skeletal muscle.

• Journal of Advanced Information Technology and Convergence
• /
• v.10 no.1
• /
• pp.25-36
• /
• 2020

Motivation: Fibers as the extracellular filamentous structures determine the shape of the cytoskeletal structures. Their characterization and reconstruction from a 3D cellular image represent very useful quantitative information at the cellular level. In this paper, we presented a novel automatic method to extract fiber diameter distribution through a pipeline to reconstruct fibers from 3D fluorescence confocal images. The pipeline is composed of four steps: segmentation, skeletonization, template fitting and fiber tracking. Segmentation of fiber is achieved by defining an energy based on tensor voting framework. After skeletonizing segmented fibers, we fit a template for each seed point. Then, the fiber tracking step reconstructs fibers by finding the best match of the next fiber segment from the previous template. Thus, we define a fiber as a set of templates, based on which we calculate a diameter distribution of fibers.

• Transactions of the Korean Society of Mechanical Engineers A
• /
• v.22 no.4
• /
• pp.826-833
• /
• 1998

The energy-absorbing characteristic of impact limiters affects the cask design so significantly that it should be evaluated as accurate as possible. The objective of this study is to find the influence of the impact limiter's steel case and gusset plates which enclose the shock absorbing cellular material on the impact energy absorption. The influence of impact limiter's steel case and gusset plate stiffeners on the impact energy absorption behavior under horizontal drop impact was evaluated for a radioactive isotope transport cask. Though the impact limiters mitigate the impact damage of the cask, the impact limiter's steel case and gusset plate stiffeners increase the impact force so significantly that should be designed as soft as possible. The impact analysis without considering impact limiter's steel case and gusset plates stiffener gives non-conservative results, so the stiffness of the steel case and gusset plates should be considered in impact analysis.

• Biomolecules & Therapeutics
• /
• v.25 no.5
• /
• pp.511-518
• /
• 2017

Ultraviolet (UV) irradiation is a relevant environment factor to induce cellular senescence and photoaging. Both autophagy- and silent information regulator T1 (SIRT1)-dependent pathways are critical cellular processes of not only maintaining normal cellular functions, but also protecting cellular senescence in skin exposed to UV irradiation. In the present studies, we investigated whether modulation of autophagy induction using a novel synthetic SIRT1 activator, heptasodium hexacarboxymethyl dipeptide-12 (named as Aquatide), suppresses the UVB irradiation-induced skin aging. Treatment with Aquatide directly activates SIRT1 and stimulates autophagy induction in cultured human dermal fibroblasts. Next, we found that Aquatide-mediated activation of SIRT1 increases autophagy induction via deacetylation of forkhead box class O (FOXO) 1. Finally, UVB irradiation-induced cellular senescence measured by $SA-{\beta}-gal$ staining was significantly decreased in cells treated with Aquatide in parallel to occurring SIRT1 activation-dependent autophagy. Together, Aquatide modulates autophagy through SIRT1 activation, contributing to suppression of skin aging caused by UV irradiation.

• The Journal of Korean Institute of Electromagnetic Engineering and Science
• /
• v.15 no.10 s.89
• /
• pp.1011-1017
• /
• 2004

Ultra Wideband(UWB) technologies have been developed to exploit a new spectrum resource in substances and to realize ultra-high-speed communication, high precision geolocation, and other applications. The energy of UWB signal is extremely spread from near DC to a few GHz. This means that the interference between conventional narrowband systems and UWB systems is inevitable. However, the interference effects had not previously been studied from UWB wireless systems to conventional mobile wireless systems sharing the frequency bands such as Korean Cellular CDMA and WCDMA. This paper experimentally evaluates the interference from two kinds of UWB sources, namely a direct-sequence spread-spectrum CDMA(DS-CDMA) UWB source and an impulse radio UWB source, to a Cellular CDMA and WCDMA digital transmission system. The average frame error rate degradation of each system are presented. From these experimental results, the interference effects of DS-CDMA UWB source is not severe compared to the Impulse UWB.

• Molecules and Cells
• /
• v.37 no.3
• /
• pp.257-263
• /
• 2014

A mammalian cell renovates itself by autophagy, a process through which cellular components are recycled to produce energy and maintain homeostasis. Recently, the abundance of gap junction proteins was shown to be regulated by autophagy during starvation conditions, suggesting that transmembrane proteins are also regulated by autophagy. Transient receptor potential vanilloid type 1 (TRPV1), an ion channel localized to the plasma membrane and endoplasmic reticulum (ER), is a sensory transducer that is activated by a wide variety of exogenous and endogenous physical and chemical stimuli. Intriguingly, the abundance of cellular TRPV1 can change dynamically under pathological conditions. However, the mechanisms by which the protein levels of TRPV1 are regulated have not yet been explored. Therefore, we investigated the mechanisms of TRPV1 recycling using HeLa cells constitutively expressing TRPV1. Endogenous TRPV1 was degraded in starvation conditions; this degradation was blocked by chloroquine (CLQ), 3MA, or downregulation of Atg7. Interestingly, a glucocorticoid (cortisol) was capable of inducing autophagy in HeLa cells. Cortisol increased cellular conversion of LC3-I to LC-3II, leading autophagy and resulting in TRPV1 degradation, which was similarly inhibited by treatment with CLQ, 3MA, or downregulation of Atg7. Furthermore, cortisol treatment induced the colocalization of GFP-LC3 with endogenous TRPV1. Cumulatively, these observations provide evidence that degradation of TRPV1 is mediated by autophagy, and that this pathway can be enhanced by cortisol.

• The Journal of the Convergence on Culture Technology
• /
• v.7 no.1
• /
• pp.558-563
• /
• 2021

Quantum-Dot Cellular Automata is a next-generation nanocircular design technology that is drawing attention from many research organizations not only because it is possible to design efficient circuits by overcoming the physical size limitations of existing CMOS circuits, but also because of its energy-efficient features. In this paper, one of the existing digital circuits, T flip-flop circuit, is proposed using QCA. The previously proposed T flip-flops are designed based on the majority gate, so the circuits are complex and have long delays. Therefore, the design of the XOR gate-based T flip-flop using cell interaction reduces circuit complexity and minimizes latency. The proposed circuit is simulated using QCADesigner, and the performance is compared and analyzed with the existing proposed circuits.

• KSII Transactions on Internet and Information Systems (TIIS)
• /
• v.14 no.12
• /
• pp.4946-4960
• /
• 2020

In a device-to-device (D2D) underlaid cellular network, there exist two types of co-channel interference. One type is inter-layer interference caused by spectrum reuse between D2D transmitters and cellular users (CUEs). Another type is intra-layer interference caused by spectrum sharing among D2D pairs. To mitigate the inter-layer interference, we first derive the interference limited area (ILA) to protect the coverage probability of cellular users by modeling D2D users' location as a Poisson point process, where a D2D transmitter is allowed to reuse the spectrum of the CUE only if the D2D transmitter is outside the ILA of the CUE. To coordinate the intra-layer interference, the spectrum sharing criterion of D2D pairs is derived based on the (signal-to-interference ratio) SIR requirement of D2D communication. Based on this criterion, D2D pairs are allowed to share the spectrum when one D2D pair is far from another sufficiently. Furthermore, to maximize the energy efficiency of the system, a resource allocation scheme is proposed according to weighted graph coloring theory and the proposed ILA restriction. Simulation results show that our proposed scheme provides significant performance gains over the conventional scheme and the random allocation scheme.

• The Journal of Korean Institute of Communications and Information Sciences
• /
• v.38A no.12
• /
• pp.1135-1144
• /
• 2013

Deploying small cells is a reliable and influential solution to handle the skyrocketing traffic increase in the cellular network, and the small cell technology is evolving to ultra-dense network (UDN). In this paper we propose a small cell on/off algorithm with a simple but essential framework composed of access point (AP), user equipment (UE), and small cell controller (SCC). We propose Device-Assisted Networking for Cellular grEening (DANCE) algorithms that save the energy consumption by tying to minimize the number of turned-on APs while maintaining the network throughput. In doing so, SCC firstly gathers the feedback messages from UEs and then makes a decision including a set of turned-on APs and user association. DANCE algorithm has several variations depending on the number of bits of the UE's feedback message (1 bit vs. N bit), and is divided into AP-first, UE-first, or Proximity ON according to the criteria of selecting the turned-on APs. We perform extensive simulations under the realistic UDN environment, and the results confirm that the proposed algorithms, compared to the baseline, can significantly enhance the energy efficiency, e.g., more than a factor of 10.

• 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.