• Proceedings of the KSR Conference
• /
• 2011.10a
• /
• pp.165-171
• /
• 2011

A Consider the dead man's switch installed in each and every locomotive cab, which support operational safety on railways around the world. The concept is very simple - every 150 to 180 seconds an illuminated push-button demands to be acknowledged so as to know that the Train Driver is alive and active. In the absence of a response over a period of minutes, the vigilance control will automatically apply the train brakes and bring the train to a stand. If we multiply the resetting of the vigilance control 60 times per hour by a 10-hour shift it equals 600 presses of the button during the shift that a Train Driver must pay attention to and acknowledge. This adds a fair bit of pressure on the train driver's job, particularly when he/she is driving through stations, with passengers moving about on platforms in an environment of complex signaling arrangements - all the while looking out for restricting signals. From this perspective, the Vigilance System's demand to be acknowledged every 150/180 seconds is disturbing and can unnecessarily take a driver's attention away from what is happening outside the confines of the cab. A much more dramatic situation can happen when a train driver is driving hour after hour at night when, by Mother's Nature request - people need to sleep. Experience and research shows that the the dead man's switch can be pressed by train driver in a state of deep relaxation and 'micro-sleep'. The vigilance control system which is applied to reduce the drive load considering bio-response multiple unit train is proposed.

• The Korean Journal of Physiology and Pharmacology
• /
• v.24 no.1
• /
• pp.69-79
• /
• 2020

Aging is one of the risk factors for the development of cardiovascular diseases. During the progression of cellular senescence, cells enter a state of irreversible growth arrest and display resistance to apoptosis. As a flavonoid, quercetin induces apoptosis in various cells. Accordingly, we investigated the relationship between quercetin-induced apoptosis and the inhibition of cellular senescence, and determined the mechanism of oxidative stress-induced vascular smooth muscle cell (VSMC) senescence. In cultured VSMCs, hydrogen peroxide (H₂O₂) dose-dependently induced senescence, which was associated with increased numbers of senescence-associated β-galactosidase-positive cells, decreased expression of SMP30, and activation of p53-p21 and p16 pathways. Along with senescence, expression of the anti-apoptotic protein Bcl-2 was observed to increase and the levels of proteins related to the apoptosis pathway were observed to decrease. Quercetin induced apoptosis through the activation of AMP-activated protein kinase. This action led to the alleviation of oxidative stress-induced VSMC senescence. Furthermore, the inhibition of AMPK activation with compound C and siRNA inhibited apoptosis and aggravated VSMC senescence by reversing p53-p21 and p16 pathways. These results suggest that senescent VSMCs are resistant to apoptosis and quercetin-induced apoptosis attenuated the oxidative stress-induced senescence through activation of AMPK. Therefore, induction of apoptosis by polyphenols such as quercetin may be worthy of attention for its anti-aging effects.

• Korean Journal of Plant Resources
• /
• v.31 no.3
• /
• pp.268-273
• /
• 2018

Hepatic ischemia-reperfusion injury (HIRI) is linked with high mortality rate. Several agents have been developed so far to reduce the risk of HIRI. In this study, we investigated the effects of combined treatment of Ginko biloba leaves extract and vitamin C (GLEVC) on hepatic ischemia-reperfusion injury. To explore the protective effects of GLEVC on HIRI rats model were tested. After the development of HIRI by using clamping method rats were then randomly divided into four groups. Different doses of GLEVC were administered in HIRI rat model. The level of ALT, AST, SOD and MDA content in serum were detected in HIRI groups. Moreover, the activity of SOD, content of MDA, and GSH in hepatic tissue were also examined. Bcl-2 and Bax protein expression were detected by immunohistochemical staining method. Compared with sham group, GLEVC has the protective effect on the HIRI-induced model. Level of ALT, AST, and MDA in blood were significantly lower in GLEVC group compared with HIRI-induced group. Moreover, SOD activity and GSH were increased in GLEVC group whereas MDA content was reduced by GLEVC treatment. Furthermore, HIRI-induced Bax protein was reduced upon GLEVC treatment, whereas Bcl-2 protein expression was enhanced. These results demonstrate that GLEVC treatment may provide potential ameliorative therapy by reducing damaged signaling mechanism in hepatic ischemia/reperfusion injury model.

• Journal of Korea Multimedia Society
• /
• v.8 no.3
• /
• pp.372-378
• /
• 2005

When a mobile node changes a sub network using Mobile IP, it must register its current location to the home agent. If a mobile node is far from its home network, the Binding Update (BU) time delay is longer and affects its connection state. To solve such a BU delay problem, a new component in HMIPv6, called MAP, supports the mobility of mobile node to reduce the signaling delay in handover However, in hierarchical MAP architecture, the register concentration to a specific MAP may be occurred, which affects the network management wholly. In this paper, we propose a MAP selection scheme based on ioad balancing by the mobility factor and the traffic property. By the mobility factor and the traffic property, a mobile node can select a adequate MAP on its mobility factor and traffic characteristic.

• BMB Reports
• /
• v.44 no.4
• /
• pp.267-272
• /
• 2011

ZAS3 is a large zinc finger transcription repressor that binds the ${\kappa}B$-motif via two signature domains of ZASN and ZASC. A loss-of-function study showed that lack of ZAS3 protein induced accelerated cell proliferation and tumorigenesis. Conversely, gain-of-function studies showed that ZAS3 repressed $NF{\kappa}B$-activated transcription by competing with $NF{\kappa}B$ for the ${\kappa}B$-motif. Based on these observations, we hypothesize that ZAS3 promotes apoptosis by interrupting anti-apoptotic activity of $NF{\kappa}B$. Here, we present evidence that upon $TNF{\alpha}$ stimulation, ZAS3 inhibits $NF{\kappa}B$-mediated cell survival and promotes caspase-mediated apoptosis. The inhibitory effect of ZAS3 on $NF{\kappa}B$ activity is mediated by neither direct association with $NF{\kappa}B$ nor disrupting nuclear localization of $NF{\kappa}B$. Instead, ZAS3 repressed the expression of two key anti-apoptotic genes of $NF{\kappa}B$, TRAF1 and TRAF2, thereby sensitizing cells to $TNF{\alpha}$-induced cell death. Taken together, our data suggest that ZAS3 is a tumor suppressor gene and therefore serves as a novel therapeutic target for developing anti-cancer drugs.

• The Journal of the Korea institute of electronic communication sciences
• /
• v.14 no.6
• /
• pp.1061-1068
• /
• 2019

Cooperative networks transmit signals form the source node to the destination node via several relay node where the combining and demodulation of relay aided signals provide the benefit of performance enhancement and data rate increment. In general, a repetitive manner transmission scheme in which the received signal from the source node is amplified/re-generated and forward to the destination node is widely used. In this paper, we analyzed the performance of cooperative networks using the mixed transmission scheme. The conventional modulation scheme is used in the source-relay links, and space-time code is applied in the relay-destination links. To reduce the complexity of the overall system, we adopt differential modulation which bypasses channel state information. We analyze bit error rate (BER) of the proposed system by considering the number of relay nodes, and the performances depending on the strength of transmission signal in the source-relays and rely-destination links are compared. In addition, we also discuss the system performance with the signal strength and the number of relay nodes simultaneously.

• Journal of the Institute of Electronics Engineers of Korea TC
• /
• v.47 no.2
• /
• pp.25-33
• /
• 2010

Introducing the quantized channel state information (CSI), space division multiple access (SDMA) can extract the multiplexing gain with the limited feedback burden. However, huge signaling burden of feedback can still suffer SDMA system because the total feedback data of SDMA is linearly dependent on the number of users. Hence, we propose a new feedback scheme to control the feedback load decided by the number of users. In this scheme, the cut-off level, which restricts the feedbacks of poor conditioned users, is suggested for the reduction of the feedback burden without the performance loss. From simulation results, then, we show that the proposed feedback scheme can achieve not only the sum-rate gain but also the reasonable feedback reduction.

• Molecules and Cells
• /
• v.41 no.11
• /
• pp.971-978
• /
• 2018

The stem cell factor (SCF)/c-KIT axis plays an important role in the hematopoietic differentiation of human pluripotent stem cells (hPSCs), but its regulatory mechanisms involving microRNAs (miRs) are not fully elucidated. Here, we demonstrated that supplementation with SCF increases the hematopoietic differentiation of hPSCs via the interaction with its receptor tyrosine kinase c-KIT, which is modulated by miR-221 and miR-222. c-KIT is comparably expressed in undifferentiated human embryonic and induced pluripotent stem cells. The inhibition of SCF signaling via treatment with a c-KIT antagonist (imatinib) during hPSC-derived hematopoiesis resulted in reductions in the yield and multi-lineage potential of hematopoietic progenitors. We found that the transcript levels of miR-221 and miR-222 targeting c-KIT were significantly lower in the pluripotent state than they were in terminally differentiated somatic cells. Furthermore, suppression of miR-221 and miR-222 in undifferentiated hPSC cultures induced more hematopoiesis by increasing c-KIT expression. Collectively, our data implied that the modulation of c-KIT by miRs may provide further potential strategies to expedite the generation of functional blood cells for therapeutic approaches and the study of the cellular machinery related to hematologic malignant diseases such as leukemia.

• Korean Journal of Plant Resources
• /
• v.30 no.6
• /
• pp.647-653
• /
• 2017

Hepatic ischemia-reperfusion injury (HIRI) is linked with high mortality rate. Several agents have been developed so far to reduce the risk of HIRI. In this study, we investigated the effects of Acanthopanax senticosus extract (AS) on hepatic ischemia-reperfusion. To explore the protective effects of A. senticosus extract injection (ASI) on hepatic ischemia-reperfusion injury rats animal model were used. After the development of HIRI by using clamping method rats were then randomly divided into five groups. Different doses of AS were administered in HIRI rat model. The level of ALT, AST, and MDA content in serum were detected in sham and HIRI groups. The activity of SOD, MPO and $Ca^{2+}-ATPase$, content of MDA, and cAMP in hepatic tissue were also measured. Expression of Bcl-2 and Bax protein were detected by immunohistochemical staining method. Compared with sham group, ASI has the protective effect on the HIRI model in rats. Blood levels of ALT, AST, SOD, MPO, and MDA were significantly lower in ASI group compared with HIRI. Indeed SOD and $Ca^{2+}-ATPase$ activities, MDA content, and cAMP level were improved in ASI group. Furthermore, Bcl-2 and Bax protein were improved in ASI group compared with only HIRI group. These results suggest that AS may provide potential ameliorative therapy by inhibiting the damage signaling mechanism in hepatic ischemia/reperfusion injury model.

• Asian Pacific Journal of Cancer Prevention
• /
• v.14 no.10
• /
• pp.5589-5597
• /
• 2013

The aim of this review article was to evaluate the relationship and the possible etiological mechanisms between endometriosis, leiomyoma (LM) and adenomyosis and gynecological cancers, such as ovarian and endometrial cancer and leiomyosarcoma (LMS). MEDLINE was searched for all articles written in the English literature from July 1966 to May 2013. Reports were collected systematically and all the references were also reviewed. Malignant transformation of gynecologic benign diseases such as endometriosis, adenomyosis and LM to ovarian and endometrial cancer remains unclear. Hormonal factors, inflammation, familial predisposition, genetic alterations, growth factors, diet, altered immune system, environmental factors and oxidative stress may be causative factors in carcinogenesis. Early menarche, low parity, late menopause and infertility have also been implicated in the pathogenesis of these cancers. Ovarian cancers and endometriosis have been shown to have common genetic alterations such as loss of heterozygosity (LOH), PTEN, p53, ARID1A mutations. MicroRNAs have also been implicated in malignant transformation. Inflammation releases proinflammatory cytokines, and activates tumor associated macrophages (TAMS) and nuclear factor kappa b (NF-KB) signaling pathways that promote genetic mutations and carcinogenesis. MED12 mutations in LM and smooth muscle tumors of undetermined malignant potential (STUMP) may contribute to malignant transformation to LMS. A hyperestrogenic state may be shared in common with pathogenesis of adenomyosis, LM and endometrial cancer. However, the effect of these benign gynecologic diseases on endometrial cancer should be studied in detail. This review study indicates that endometriosis, LM, adenomyosis may be associated with increased risk of gynecological cancers such as endometrial and ovarian cancers. The patients who have these gynecological benign diseases should be counseled about the future risks of developing cancer. Further studies are needed to investigate the relationship between STUMPs, LMS and LM and characteristics and outcome endometrial carcinoma in adenomyotic patients.