• KSII Transactions on Internet and Information Systems (TIIS)
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• v.13 no.8
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• pp.3821-3841
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• 2019

Cloud radio access networks (C-RANs) have been regarded in recent times as a promising concept in future 5G technologies where all DSP processors are moved into a central base band unit (BBU) pool in the cloud, and distributed remote radio heads (RRHs) compress and forward received radio signals from mobile users to the BBUs through radio links. In such dynamic environment, automatic decision-making approaches, such as artificial intelligence based deep reinforcement learning (DRL), become imperative in designing new solutions. In this paper, we propose a generic framework of autonomous cell activation and customized physical resource allocation schemes for energy consumption and QoS optimization in wireless networks. We formulate the problem as fractional power control with bandwidth adaptation and full power control and bandwidth allocation models and set up a Q-learning model to satisfy the QoS requirements of users and to achieve low energy consumption with the minimum number of active RRHs under varying traffic demand and network densities. Extensive simulations are conducted to show the effectiveness of our proposed solution compared to existing schemes.

• BMB Reports
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• v.34 no.3
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• pp.212-218
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• 2001

Although the blockage of a cell cycle by specific inhibitors of $Ca^{2+}/$calmodulin-dependent protein kinase II (CaMK-II) is well known, the activity profile of CaMK-II during the cell cycle in the absence of any direct effectors of the enzyme is unclear. The activity of native CaMK-II in NIH 3T3 cells was examined by the use of cell cycle-specific arresting and synchronizing methods. The total catalytic activity of CaMK-II in arrested cells was decreased about 30% in the M phase, whereas the $Ca^{2+}$-independent autonomous activity increased about 1.5-fold in the M phase and decreased about 50% at the G1/S transition. The in vivo phosphorylation level of CaMK-II was lowest at G1/S and highest in M. The CaMK-II protein level was unchanged during the cell cycle. When the cells were synchronized, the autonomous activity was increased only in M. These results indicate that the physiologically relevant portion of CaMK-II is activated only in M, and that the net activation of CaMK-II is required in mitosis.

• ETRI Journal
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• v.40 no.3
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• pp.318-329
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• 2018

Femtocell (FC) technology envisaged as a cost-effective approach to attain better indoor coverage of mobile voice and data service. Deployment of FCs over macrocell forms a heterogeneous network. In urban areas, the key factor limits the successful deployment of FCs is inter-cell interference (ICI), which severely affects the performance of victim users. Autonomous FC transmission power setting is one straightforward way for coordinating ICI in the downlink. Application of intelligent control using soft computing techniques has not yet explored well for wireless networks. In this work, autonomous FC transmission power setting strategy using Adaptive Neuro Fuzzy Inference System is proposed. The main advantage of the proposed method is zero signaling overhead, reduced computational complexity and bare minimum delay in performing power setting of FC base station because only the periodic channel measurement reports fed back by the user equipment are needed. System level simulation results validate the effectiveness of the proposed method by providing much better throughput, even under high interference activation scenario and cell edge users can be prevented from going outage.

• Korean Journal of Animal Reproduction
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• v.24 no.1
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• pp.41-47
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• 2000

Gonadotropin receptors are members of the seven-transmembrane (TM) receptor family, Point mutations in the lutropin/choriogonadotropin receptor (LH/CGR) have been shown to cause constitutive activation which results in precocious puberty in affected males, We introduced one of the mutation, D556Y, into the LH/CG receptor and the same high affinity binding mutant (D556Y) receptor clone cell for wild type LH/CGR (LH/CGR-wt) was chosen for further analysis, In contrast to cells expressing LH/CGR-wt, it was demonstrated that the mutant receptor exhibited markedly increased basal cAMP production in the absence of agonist, suggesting that autonomous Leydig cell activity in familial male-precocious puberty (FMPP) is caused by a constitutively activating LH/CGR.

• Molecules and Cells
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• v.43 no.2
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• pp.198-202
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• 2020

Comprehensive inhibition of RUNX1, RUNX2, and RUNX3 led to marked cell suppression compared with inhibition of RUNX1 alone, clarifying that the RUNX family members are important for proliferation and maintenance of diverse cancers, and "cluster regulation of RUNX (CROX)" is a very effective strategy to suppress cancer cells. Recent studies reported by us and other groups suggested that wild-type RUNX1 is needed for survival and proliferation of certain types of leukemia, lung cancer, gastric cancer, etc. and for their one of metastatic target sites such as born marrow endothelial niche, suggesting that RUNX1 often functions oncogenic manners in cancer cells. In this review, we describe the significance and paradoxical requirement of RUNX1 tumor suppressor in leukemia and even solid cancers based on recent our findings such as "genetic compensation of RUNX family transcription factors (the compensation mechanism for the total level of RUNX family protein expression)", "RUNX1 inhibition-induced inhibitory effects on leukemia cells and on solid cancers through p53 activation", and "autonomous feedback loop of RUNX1-p53-CBFB in acute myeloid leukemia cells". Taken together, these findings identify a crucial role for the RUNX cluster in the maintenance and progression of cancers and suggest that modulation of the RUNX cluster using the pyrrole-imidazole polyamide gene-switch technology is a potential novel therapeutic approach to control cancers.

• Journal of the Korean Institute of Intelligent Systems
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• v.13 no.2
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• pp.169-174
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• 2003

The trial and success of malicious cyber attacks has been increased rapidly with spreading of Internet and the activation of a internet shopping mall and the supply of an online, or an offline internet, so it is expected to make a problem more and more. The goal of intrusion detection is to identify unauthorized use, misuse, and abuse of computer systems by both system insiders and external penetrators in real time. In fact, the general security system based on Internet couldn't cope with the attack properly, if ever. other regular systems have depended on common vaccine softwares to cope with the attack. But in this paper, we will use the positive selection and negative selection mechanism of T-cell, which is the biologically distributed autonomous system, to develop the self/nonself recognition algorithm and AIS (Artificial Immune System) that is easy to be concrete on the artificial system. For making it come true, we will apply AIS to the network environment, which is a computer security system.

• Journal of the Korean Institute of Intelligent Systems
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• v.12 no.5
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• pp.411-416
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• 2002

Recently, the trial and success of malicious cyber attacks has been increased rapidly with spreading of Internet and the activation of a internet shopping mall and the supply of an online internet, so it is expected to make a problem more and more. Currently, the general security system based on Internet couldn't cope with the attack properly, if ever, other regular systems have depended on common softwares to cope with the attack. In this paper, we propose the positive selection mechanism and negative selection mechanism of T-cell, which is the biological distributed autonomous system, to develop the self/non-self recognition algorithm, the anomalous behavior detection algorithm, and AIS (Artificial Immune System) that is easy to be concrete on the artificial system. The proposed algorithm can cope with new intrusion as well as existing one to intrusion detection system in the network environment.

• Proceedings of the Korean Society of Developmental Biology Conference
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• 2003.10a
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• pp.83-83
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• 2003

The lutropin/choriogonadotropin receptor (LHR) is a member of the rhodopsin-like subfamily of G protein coupled receptor (GPCRs), that has been shown to mediate the internalization of its two naturally occurring agonist, lutropin and choriogonadotropin (CG). The clustered agonist-receptor complex is internalized by a dynamin-dependent pathway and traverses the endosomal compartment without agonist dissociation Dissociation of the agonist-receptor complex occurs in the lysosomes, where both the agonist and receptor are degrade. Recently, constitutively activating mutations of the receptor have been identified that are associated with familial male-precocious puberty (FMPP). A FMPP is a form of sexual precocious puberty in boys in which testosterone levels are elevated independent of changes in luteinizing hormone-releasing hormone and serum luteinizing hormone levels, We have now analyzed two naturally occurring, constitutively active mutants of the human LHR. These mutations were introduced into the rat LHR (rLHR) and are designated L435R and D556Y. Cells expressing rLHR-D556Y bind human choriogonadotropin (hCG) with normal affinity, exhibit a 25-fold increase in basal cAMP and respond to hCG with a normal increase in cAMP accumulation. Cells expressing rLHR-L435R also bind hCG with normal affinity, exhibit a 47-fold increase in basal cAMP, and do not respond to hCG with a further increase in cAMP accumulation. This mutation enhances the internalization of the free and agonist-occupied receptors ~2- and ~17- fold, respectively We conclude that the state of activation of the rLHR can modulate its basal and/or agonist-stimulated internalization. Since the internalization of hCG is involved in the termination of hCG actions, we suggest that the lack of responsiveness detected in cells expressing rLHR-L435R is due to the fast rate of internalization of the bound hCG. The finding that membranes expressing rLHR-L435R respond to hCG with an increase in adenylyl cyclase activity supports this suggestion. Autonomous Leydig cell activity in FMPP is caused by a constitutively activating LH/CGR.

• Animal Bioscience
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• v.36 no.7
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• pp.1022-1033
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• 2023

Objective: p66Shc, a 66 kDa protein isoform encoded by the proto-oncogene SHC, is an essential intracellular redox homeostasis regulatory enzyme that is involved in the regulation of cellular oxidative stress, apoptosis induction and the occurrence of multiple age-related diseases. This study investigated the expression profile and functional characteristics of p66Shc during preimplantation embryo development in sheep. Methods: The expression pattern of p66Shc during preimplantation embryo development in sheep at the mRNA and protein levels were studied by quantitative real-time polymerase chain reaction (RT-qPCR) and immunofluorescence staining. The effect of p66Shc knockdown on the developmental potential were evaluated by cleavage rate, morula rate and blastocyst rate. The effect of p66Shc deficiency on reactive oxygen species (ROS) production, DNA oxidative damage and the expression of antioxidant enzymes (e.g., catalase and manganese superoxide dismutase [MnSOD]) were also investigated by immunofluorescence staining. Results: Our results showed that p66Shc mRNA and protein were expressed in all stages of sheep early embryos and that p66Shc mRNA was significantly downregulated in the 4-to 8-cell stage (p<0.05) and significantly upregulated in the morula and blastocyst stages after embryonic genome activation (EGA) (p<0.05). Immunofluorescence staining showed that the p66Shc protein was mainly located in the peripheral region of the blastomere cytoplasm at different stages of preimplantation embryonic development. Notably, serine (Ser36)-phosphorylated p66Shc localized only in the cytoplasm during the 2- to 8-cell stage prior to EGA, while phosphorylated (Ser36) p66Shc localized not only in the cytoplasm but also predominantly in the nucleus after EGA. RNAi-mediated silencing of p66Shc via microinjection of p66Shc siRNA into sheep zygotes resulted in significant decreases in p66Shc mRNA and protein levels (p<0.05). Knockdown of p66Shc resulted in significant declines in the levels of intracellular ROS (p<0.05) and the DNA damage marker 8-hydroxy2'-deoxyguanosine (p<0.05), markedly increased MnSOD levels (p<0.05) and resulted in a tendency to develop to the morula stage. Conclusion: These results indicate that p66Shc is involved in the metabolic regulation of ROS production and DNA oxidative damage during sheep early embryonic development.