• Molecules and Cells
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• v.40 no.9
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• pp.607-612
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• 2017

When mammalian cells and animals face a variety of internal or external stresses, they need to make homeostatic changes so as to cope with various stresses. To this end, mammalian cells are equipped with two critical stress responses, autophagy and cellular senescence. Autophagy and cellular senescence share a number of stimuli including telomere shortening, DNA damage, oncogenic stress and oxidative stress, suggesting their intimate relationship. Autophagy is originally thought to suppress cellular senescence by removing damaged macromolecules or organelles, yet recent studies also indicated that autophagy promotes cellular senescence by facilitating the synthesis of senescence-associated secretory proteins. These seemingly opposite roles of autophagy may reflect a complex picture of autophagic regulation on cellular senescence, including different types of autophagy or a unique spatiotemporal activation of autophagy. Thus, a better understanding of autophagy process will lead us to not only elucidate the conundrum how autophagy plays dual roles in the regulation of cellular senescence but also helps the development of new therapeutic strategies for many human diseases associated with cellular senescence. We address the pro-senescence and anti-senescence roles of autophagy while focusing on the potential mechanistic aspects of this complex relationship between autophagy and cellular senescence.

• Molecules and Cells
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• v.39 no.1
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• pp.6-19
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• 2016

Redox signalling comprises the biology of molecular signal transduction mediated by reactive oxygen (or nitrogen) species. By specific and reversible oxidation of redoxsensitive cysteines, many biological processes sense and respond to signals from the intracellular redox environment. Redox signals are therefore important regulators of cellular homeostasis. Recently, it has become apparent that the cellular redox state oscillates in vivo and in vitro, with a period of about one day (circadian). Circadian timekeeping allows cells and organisms to adapt their biology to resonate with the 24-hour cycle of day/night. The importance of this innate biological timekeeping is illustrated by the association of clock disruption with the early onset of several diseases (e.g. type II diabetes, stroke and several forms of cancer). Circadian regulation of cellular redox balance suggests potentially two distinct roles for redox signalling in relation to the cellular clock: one where it is regulated by the clock, and one where it regulates the clock. Here, we introduce the concepts of redox signalling and cellular timekeeping, and then critically appraise the evidence for the reciprocal regulation between cellular redox state and the circadian clock. We conclude there is a substantial body of evidence supporting circadian regulation of cellular redox state, but that it would be premature to conclude that the converse is also true. We therefore propose some approaches that might yield more insight into redox control of cellular timekeeping.

• Journal of applied mathematics & informatics
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• v.20 no.1_2
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• pp.433-443
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• 2006

In [1], they build two populations' cellular automata model with predation based on the Penna model. In this paper, uncertain aspects and problems of imprecise and vague data are considered in this model. A fuzzy cellular automata model containing movable wolves and sheep has been built. The results show that the fuzzy cellular automata can simulate the classical CA model and can deal with imprecise and vague data.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.122.2-122.2
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• 2002

• Journal of Korea Multimedia Society
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• v.15 no.12
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• pp.1456-1463
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• 2012

In this paper, we study the ON/OFF control policy of base stations in two-tier heterogeneous cellular networks to minimize the total power consumption of the system. Using heterogeneous cellular networks is a potential approach of providing higher throughput and coverage compared to conventional networks with only macrocell deployment, but in fact heterogeneous cellular networks often operates regardless of total power consumption, which is a very important issue of modern cellular networks. We propose a policy that controls the activation/deactivation of base stations in heterogeneous cellular networks to minimize total power consumption. Under this policy, the total power consumed can be significantly reduced when the traffic is low while the QoS requirement is satisfied.

• The Transactions of the Korean Institute of Electrical Engineers D
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• v.49 no.8
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• pp.481-490
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• 2000

This paper analyzes interference power, Erlang capacity, the number of handoff occurrences, and call blocking probability with respect to the cell radius, the soft handoff region, and the mobile's velocity in a CDMA hierarchical cellular system. The microcell cellular system has the higher Erlang capacity than the macrocell cellular system. However, the microcell cellular system, which has a high system capacity through frequency reuse has the call blocking probability higher than macrocell cellular system. Also the interference power and the call blocking probability are decreased with the operation of soft handoff. Therefore, this paper presents the optimization of soft handoff region so as to maximize system's Erlang capacity with the low the call blocking probability according to mobile's velocity in the CDMA hierarchial cellular system.

• BMB Reports
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• v.52 no.1
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• pp.35-41
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• 2019

Cellular senescence, a permanent state of cell cycle arrest, is believed to have originally evolved to limit the proliferation of old or damaged cells. However, it has been recently shown that cellular senescence is a physiological and pathological program contributing to embryogenesis, immune response, and wound repair, as well as aging and age-related diseases. Unlike replicative senescence associated with telomere attrition, premature senescence rapidly occurs in response to various intrinsic and extrinsic insults. Thus, cellular senescence has also been considered suppressive mechanism of tumorigenesis. Current studies have revealed that therapy-induced senescence (TIS), a type of senescence caused by traditional cancer therapy, could play a critical role in cancer treatment. In this review, we outline the key features and the molecular pathways of cellular senescence. Better understanding of cellular senescence will provide insights into the development of powerful strategies to control cellular senescence for therapeutic benefit. Lastly, we discuss existing strategies for the induction of cancer cell senescence to improve efficacy of anticancer therapy.

• Microbiology and Biotechnology Letters
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• v.49 no.4
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• pp.478-484
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• 2021

Cellular resources including transcriptional and translational machineries in bacteria are limited, yet microorganisms depend upon them to maximize cellular fitness. Bacteria have evolved strategies for using resources economically. Regulatory networks for the gene expression system enable the cell to synthesize proteins only when necessary. At the same time, regulatory interactions enable the cell to limit losses when the system cannot make a cellular profit due to fake substrates. Also, the architecture of the gene expression flow can be advantageous for clustering functionally related products, thus resulting in effective interactions among molecules. In addition, cellular systems modulate the investment of proteomes, depending upon nutrient qualities, and fast-growing cells spend more resources on the synthesis of ribosomes, whereas nonribosomal proteins are synthesized in nutrient-limited conditions. A deeper understanding of cellular mechanisms underlying the optimal allocation of cellular resources can be used for biotechnological purposes, such as designing complex genetic circuits and constructing microbial cell factories.

• Journal of the Chungcheong Mathematical Society
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• v.21 no.4
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• pp.447-454
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• 2008

In this short note, we will point out and modify some logical errors in literatures about the theory of cellular automata.

• ETRI Journal
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• v.40 no.2
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• pp.207-217
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• 2018

As implementation of the in-band full duplex (IFD) transceiver becomes feasible, research interest is growing with respect to using IFD communication with cellular networks. However, the cellular network in which the IFD communication is applied inevitably suffers from an increase of the co-channel interference (CCI) due to IFD simultaneous transmission and reception. In this paper, we analyze the performance of a cellular network based on uni-directional IFD (UD-IFD) communication, wherein an IFD base station simultaneously supports downlink and uplink transmissions of half-duplex (HD) users. In addition, a multi-pair CCI cancellation (MP-CCIC) method combining CCIC and user pairing is proposed to improve the performance of the UD-IFD network. Simulation results showed that, compared to a conventional HD cellular network without using CCIC, capacity gain was not obtained in the UD-IFD cellular network. On the other hand, when applying the proposed MP-CCIC, the capacity of the UD-IFD cellular network greatly improved compared to that of an HD cellular network.