• IMMUNE NETWORK
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• v.24 no.1
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• pp.11.1-11.18
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• 2024

IL-15 belongs to the common gamma chain cytokine family and has pleiotropic immunological functions. IL-15 is a homeostatic cytokine essential for the development and maintenance of NK cells and memory CD8⁺ T cells. In addition, IL-15 plays a critical role in the activation, effector functions, tissue residency, and senescence of CD8⁺ T cells. IL-15 also activates virtual memory T cells, mucosal-associated invariant T cells and γδ T cells. Recently, IL-15 has been highlighted as a major trigger of TCR-independent activation of T cells. This mechanism is involved in T cell-mediated immunopathogenesis in diverse diseases, including viral infections and chronic inflammatory diseases. Deeper understanding of IL-15-mediated T-cell responses and their underlying mechanisms could optimize therapeutic strategies to ameliorate host injury by T cell-mediated immunopathogenesis. This review highlights recent advancements in comprehending the role of IL-15 in relation to T cell responses and immunopathogenesis under various host conditions.

• JSTS:Journal of Semiconductor Technology and Science
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• v.12 no.4
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• pp.449-457
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• 2012

The program/erase (P/E) cyclic endurances including bias temperature instability (BTI) behaviors of Metal-$Al_2O_3$-Nitride-Oxide-Semiconductor (MANOS) memories are investigated in comparison with those of Semiconductor-Oxide-Nitride-Oxide-Semiconductor (SONOS) memories. In terms of BTI behaviors, the SONOS power-law exponent n is ~0.3 independent of the P/E cycle and the temperature in the case of programmed cell, and 0.36~0.66 sensitive to the temperature in case of erased cell. Physical mechanisms are observed with thermally activated $h^*$ diffusion-induced Si/$SiO_2$ interface trap ($N_{IT}$) curing and Poole-Frenkel emission of holes trapped in border trap in the bottom oxide ($N_{OT}$). In terms of the BTI behavior in MANOS memory cells, the power-law exponent is n=0.4~0.9 in the programmed cell and n=0.65~1.2 in the erased cell, which means that the power law is strong function of the number of P/E cycles, not of the temperature. Related mechanism is can be explained by the competition between the cycle-induced degradation of P/E efficiency and the temperature-controlled $h^*$ diffusion followed by $N_{IT}$ passivation.

• Journal of the Institute of Electronics and Information Engineers
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• v.50 no.4
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• pp.239-245
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• 2013

The data retention characteristics depending on neighbor cell's threshold voltage (Vt) in a multilevel NAND flash memory is studied. It is found that a Vt shift (${\Delta}Vt$) of the noted cell during a thermal retention test is increased as the number of erase-state (lowest Vt state) cells surrounding the noted cell increases. It is because a charge loss from a floating gate is originated from not only intrinsic mechanism but also lateral electric field between the neighboring cells. From the electric field simulation, we can find that the electric field is increased and it results in the increased charge loss as the device is scaled down.

• Animal cells and systems
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• v.13 no.4
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• pp.357-362
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• 2009

Hesperidin, the most abundant polyphenolic compound found in citrus fruits, has been known to possess neuroprotective, sedative, and anticonvulsive effects on the nervous system. In a recent electrophysiological study, it was reported that hesperidin induced biphasic change in population spike amplitude in hippocampal CA1 neurons in response to both single spike stimuli and theta-burst stimulation depending on its concentration. However, the precise mechanism by which hesperidin acts on neuronal functions has not been fully elucidated. Here, using whole-cell patch-clamp recording, we revealed that hesperidin did not affect excitatory synaptic activities such as basal synaptic transmission and theta-burst LTP. Moreover, in a current injection experiment, spike number, resting membrane potential and action potential threshold also remained unchanged. Taken together, these results indicate that the effects of hesperidin on the neuronal functions such as spiking activity might not be attributable to either modification of excitatory synaptic transmissions or changes in membrane excitability in hippocampal CA1 neuron.

• The Transactions of the Korean Institute of Electrical Engineers C
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• v.49 no.1
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• pp.1-7
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• 2000

The SNOSFET memory devices with ultrathin ONO(tunnel oxide-nitride-blocking oxide) gate dielectric were fabricated using n-well CMOS process and investigated its characteristics. The thicknesses of tunnel oxide, nitride and blocking oxide were $23{\AA},\; 53{\AA}\; and\; 33{\AA}$, respectively. Auger analysis shows that the ONO layer is made up of $SiO_2(upper layer of blocking oxide)/O-rich\; SiO_x\N\_y$. It clearly shows that the converting layer with $SiO_x\N\_y(lower layer of blocking oxide)/N-rich SiO_x\N\_y(nitride)/O-rich SiO_x\N\_y(tunnel oxide)$. It clearly shows that the converting layer with $SiO_x\N\_y$ phase exists near the interface between the blocking oxide and nitride. The programming condition of +8 V, 20 ms, -8 V, 50 ms is determined and data retention over 10 years is obtained. Under the condition of 8 V programming, it was confirmed that the modified Fowler-Nordheim tunneling id dominant charge transport mechanism. The programmed threshold voltage is distributed less than 0.1 V so that the reading error of memory stated can be minimized. An $8\times8$ NAND type flash EEPROM with SONOSFET memory cell was designed and simulated with the extracted SPICE parameters. The sufficient read cell current was obtained and the upper limit of $V_{TH}$ for write state was over 2V.

• YAKHAK HOEJI
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• v.49 no.2
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• pp.168-173
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• 2005

Alzheimers disease (AD) is the most prevalent form of neurodegenerations associated with aging in the human population. This disease is characterized by the extracellular deposition of beta-amyloid (A ${\beta}$) peptide in cerebral plaques. The A ${\beta}$ peptide is derived from the ${\beta}$-amyloid precursor protein ( ${\beta}$APP). Photolytic processing of ${\beta}$APP by ${\beta}$-secretase(beta-site APP-cleaving enzyme, BASE) and ${\gamma}$-secretase generates the A ${\beta}$ peptide. Several lines of evidence support that A ${\beta}$-induced neuronal cell death is major mechanisms of development of AD. Accordingly, the ${\beta}$-and ${\gamma}$-secretase have been implicated to be excellent targets for the treatment of AD. We previously found that sesaminol glucosides have improving effect on memory functions through anti-oxidative mechanism. In this study, to elucidate possible other mechanism (inhibition of ${\beta}$-and ${\gamma}$-secretase) of sesaminol glucosides, we examined the improving effect of sesaminol glucosides in the scopolamine (1 mg/kg/mouse)-induced memory dysfunction using water maze test in the mice. Sesaminol glucosides (3.75, 7.5 mg/kg/6ml/day p.o., for 3 weeks) reversed the latency time, distance and velocity by scopolamine in dose dependent manner. Next, ${\beta}$-and ${\gamma}$-secretase activities were determined in different regions of brain. Sesaminol glucosides dose-dependently attenuated scopolamine-induced ${\beta}$-secretase activities in cortex and hippocampous and ${\gamma}$-secretase in cortex. This study therefore suggests that sesaminol glucosides may be a useful agent for prevention of the development or progression of AD, and its inhibitory effect on secretase may play a role in the improving action of sesaminol glucosides on memory function.

• The Korea Journal of Herbology
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• v.30 no.1
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• pp.67-75
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• 2015

Objectives : The aim of this study is to examine the neuroprotective effect of wheat bran extract (WBE) against ${\beta}$-amyloid ($A{\beta}$)-induced apoptotic cell death in SH-SY5Y human neuroblastoma cells and memory impairment in triple transgenic animal model's of Alzheimer's disease (3xTg AD mice). Methods : In SH-SY5Y cells, MTT assay and TUNEL staining were conducted to evaluate the protective effect of WBE against $A{\beta}_{25-35}$-induced neurotoxicity and apoptosis. Alterations in mitochondrial transmembrane potential (MMP), expression of proapoptotic Bax and antiapoptotic Bcl-2 proteins, cleavage of PARP, and brain-derived neurotrophic factor (BDNF) levels were analyzed to elucidate the neuroprotective mechanism of WBE. To further investigate the memory enhancing effect of WBE, Morris water maze test was performed in 3xTg AD mice. Results : In SH-SY5Y cells, WBE protected against $A{\beta}_{25-35}$-caused cytotoxicity and apoptosis as shown by the restoration of cell viability in MTT assay and inhibition of DNA fragmentation in TUNEL staining. $A{\beta}_{25-35}$-induced apoptotic signals such as dissipation of MMP, decreased Bcl-2/Bax ratio, and cleavage of PARP were suppressed by WBE. Moreover, WBE up-regulated the protein levels of BDNF, which seemed to be mediated by activation of cAMP response element-binding protein (CREB). In 3xTg AD mice, oral administration of WBE attenuated learning and memory deficit as verified by reduced mean escape latency in water maze test. Conclusions : WBE protects neuronal cells from $A{\beta}_{25-35}$-induced apoptotic cell death and restores learning and memory impairments in 3xTg AD mice. These findings suggest that WBE exhibit neuroprotective potential for the management of AD.

• Proceedings of the Korean Institute of Intelligent Systems Conference
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• 2002.12a
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• pp.113-117
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• 2002

PID controllers, which have been widely used in industry, have a simple structure and robustness to modeling error. But it is difficult to have uniformly good control performance in system parameters variation or different velocity command. In this paper, we propose a nonlinear adaptive PR controller based on an Immune feedback mechanism and a gradient descent teaming. This algorithm has a simple structure and robustness to system parameters variation. To verify performances of the proposed nonlinear adaptive PID controller, the speed control of nonlinear DC motor Is peformed. The simulation results show that the proposed control systems are effective in tracking a command velocity under system parameters variation

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.5
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• pp.1025-1034
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• 2002

The herbal extract (YMT_02) is a modified herbal extracts from Yukmijihwang-tang (YMJ) to promote memory-enhancing. The YMJ extracts has been widely used as an anti-aging herbal medicine for hundred years in Asian countries. The purpose of this study is to; 1) quantitatively evaluate the memory-enhancing effect of YMT_02 by behavior task, 2) identify candidate genes responsible for enhancing memory by cDNA microarray and 3) assess the anti-oxidant effect of YMT_02 on PC12 cell. Memory retention abilities are addressed by passive avoidance task with Sprague-Dawley (SD) male rat. Before the training session, the rats are subdivided into four groups and administrated with YMT_02, Ginkgo biloba, Soya lecithin and normal saline for 10 days. The retention test was performed. 24 hours after the training session. The retention time of the YMT_02 group was significantly (p<0.05) delayed (～100%), whereas Ginkgo biloba and Soya lecithin treatment delayed 20% and 10% respectively. The hippocampi of YMT_02 and control group were dissected and mANA was further purified. After synthesizing cDNA using oligo-dT primer, the cDNA were applied to Incyte rat GEMTM 2 cDNA microarray. The microarray results show that prealbumin(transthyretin), phosphotidylethanolamine N-methyltransferase, and PEP-19 are expressed abundantly in the YMT_02 treated group. Especially, PEP-19 is a neuron-specific protein, which inhibits apoptotic processes in neuronal cell. On the other hand, transcripts of RAB15, glutamate receptor subunit 2 and CDK108 are abundant in control group. Besides, neuronal genes involved in neuronal death or neurodegeneration such as neuronal-pentraxin and spectrin are abundantly expressed in control group. Additionally, the YMT_02 shows an anti oxidative effect in the PC12 cell. The list of differentially expressed genes may implicate further insight on the action and mechanism behind the memory-enhancing effect of herbal extracts YMT_02, for example, anti-apoptotic, anti-oxidative, and neuroprotective effects.

• The Korea Journal of Herbology
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• v.30 no.2
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• pp.43-48
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• 2015

Objectives : The aim of this study was to investigate the memory enhancing properties of extract of Hoelen Cum Radix (HCR) and its possible mechanism in mice of normal condition. Methods : We evaluated the effects of HCR on cognitive function and memory enhancement in normal mice. Male ICR mice were orally administrated with HCR 100 mg/kg for 7 days and equal volume of saline was administrated to the control group in the same condition. We conducted two behavioral tests which measure the spatial working memory (Y-maze test) and cognitive fear memory (passive avoidance test). We also investigated whether HCR affects the hippocampal neurogenesis in the brain. To assess the effects of HCR on neural progenitor cell differentiation and neurite outgrowth in the early stage of hippocampal neurogenesis, we performed doublecortin (DCX), a direct neurogenesis marker, immunohistochemical analysis in the dentate gyrus (DG) of the mouse hippocampus. Results : HCR significantly enhanced memory and cognitive function as determined by the Y-maze test (p<0.05) and passive avoidance test (p<0.001). Moreover, HCR increased DCX positive cells (p<0.01) and neurite length (p<0.01) compared to the control group. These results indicated that HCR stimulates differentiation of neural progenitor cells and promotes neurite outgrowth in hippocampal DG of the mice. Conclusion : We concluded that HCR shows memory enhancing effects through the stimulation of hippocampal neurogenesis as a consequence of accelerated neuronal differentiation and neurite outgrowth in the DG of the hippocampus after HCR treatment.