• Proceedings of the IEEK Conference
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• 2003.11c
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• pp.172-175
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• 2003

In this paper we propose a method fur the evaluation of the quality of service for VoIP services in NGN. Specifically, let us anatomize the elements of delay of a voice connection in the network in an end-to-end manner and investigate expected value at each point. We extract the delay time in each element in the network such as gateway, network node, and terminal equipment, and estimate an upper bound fur the tolerable delay in each element.

• Anatomy and Cell Biology
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• v.56 no.1
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• pp.86-93
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• 2023

Age at death estimation has always been a crucial yet challenging part of identification process in forensic field. The use of human skeletons have long been explored using the principle of macro and micro-architecture change in correlation with increasing age. The clavicle is recommended as the best candidate for accurate age estimation because of its accessibility, time to maturation and minimal effect from weight. Our study applies pre-trained convolutional neural network in order to achieve the most accurate and cost effective age estimation model using clavicular bone. The total of 988 clavicles of Thai population with known age and sex were radiographed using Kodak 9000 Extra-oral Imaging System. The radiographs then went through preprocessing protocol which include region of interest selection and quality assessment. Additional samples were generated using generative adversarial network. The total clavicular images used in this study were 3,999 which were then separated into training and test set, and the test set were subsequently categorized into 7 age groups. GoogLeNet was modified at two layers and fine tuned the parameters. The highest validation accuracy was 89.02% but the test set achieved only 30% accuracy. Our results show that the use of medial clavicular radiographs has a potential in the field of age at death estimation, thus, further study is recommended.

• IMMUNE NETWORK
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• v.12 no.1
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• pp.18-26
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• 2012

Background: Vitamin C is an essential nutrient for maintaining human life. Vitamin C insufficiency in the plasma is closely related with the development of scurvy. However, in vivo kinetics of vitamin C regarding its storage and consumption is still largely unknown. Methods: We used $Gulo^{-/-}$ mice, which cannot synthesize vitamin C like human. Vitamin C level in plasma and organs from $Gulo^{-/-}$ mice was examined, and it compared with the level of wild-type mice during 5 weeks. Results: The significant weight loss of $Gulo^{-/-}$ mice was shown at 3 weeks after vitamin C withdrawal. However, there was no differences between wild-type and vitamin C-supplemented $Gulo^{-/-}$ mice (3.3 g/L in drinking water). The concentration of vitamin C in plasma and organs was significantly decreased at 1 week after vitamin C withdrawal. Vitamin C is preferentially deposited in adrenal gland, lymph node, lung, and brain. There were no significant changes in the numbers and CD4/CD8 ratio of splenocytes in $Gulo^{-/-}$ mice with vitamin C withdrawal for 4 weeks. And the architecture of spleen in $Gulo^{-/-}$ mice was disrupted at 5 weeks after vitamin C withdrawal. Conclusion: The vitamin C level of $Gulo^{-/-}$ mice was considerably decreased from 1 week after vitamin C withdrawal. Vitamin C is preferentially stored in some organs such as brain, adrenal gland and lung.

• Applied Microscopy
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• v.48 no.3
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• pp.55-61
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• 2018

The synaptic vesicle is a specialized structure in presynaptic terminals that stores various neurotransmitters. The actin filament has been proposed for playing an important role in mobilizing synaptic vesicles. To understand the role of actin filament on synaptic vesicle pooling, we characterized synaptic vesicles and actin filament after treatment of brain-derived neurotrophic factor (BDNF) or Latrunculin A on primary cultured neuron from rat embryo hippocampus. Western blots revealed that BDNF treatment increased the expression of synapsin I protein, but Latrunculin A treatment decreased the synapsin I protein expression. The increased expression of synapsin I after BDNF disappeared by the treatment of Latrunculin A. Three-dimensional (3D) tomography of synapse showed that more synaptic vesicles localized near the active zone and total number of synaptic vesicles increased after treatment of BDNF. But the number of synaptic vesicle was 2.5-fold reduced in presynaptic terminals and the loss of filamentous network was observed after Latrunculin A application. The treatment of Latruculin A after preincubation of BDNF group showed that synaptic vesicle number was similar to that of control group, but filamentous structures were not restored. These data suggest that the actin filament plays a significant role in synaptic vesicles pooling in presynaptic terminals.

• IMMUNE NETWORK
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• v.11 no.6
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• pp.390-398
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• 2011

Background: Epstein Barr virus (EBV) infected B cells are transformed into lymphoblastoid cell lines. Some researchers suggested some a few similarities between this process and carcinogenesis. We observed the expression of CD80 and CD86, co-stimulatory molecules on EBV-transformed B cells and changes of CD54 expression after stimulation of CD80 and CD86. Methods: CD80 and CD86 were stimulated using anti-CD80 and anti-CD86 monoclonal antibodies. To assess apoptosis and surface protein expression, flow cytometric analysis was performed. Intracellular signal molecules were evaluated by RT-PCR and immunoblot. Morphology and localization of proteins were examined using inverted or confocal microscope. Results: Cross-linking of CD80 and CD86 induced apoptosis and interfered with proliferation of EBV-transformed B cells, and dispersion of clumped cells. We also examined that their stimulation induced ROS accumulation and reduced CD54 expression. Interestingly, we observed that CD80 and CD86 diminished the expression of CD54 in different methods. Both CD80 and CD86 downregulated activation of focal adhesion kinase. CD80 stimulus inhibited CD54 expression through mainly RhoA inactivation, while CD86 down-regulated Ras and JNK phosphorylation. Conclusion: These results suggest that co-stimulatory CD80 and CD86 molecules, expressed EBV-transformed B cells, may play a role in apoptosis and cell adhesion.

• IMMUNE NETWORK
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• v.15 no.3
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• pp.161-166
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• 2015

Early growth response (Egr)-1 is a $Cys_2-His_2-type$ zincfinger transcription factor. It has been shown to induce survival and proliferation of immature and mature B cells, respectively, but its role in the differentiation of B cells into plasma cells remains unclear. To examine the effects of Egr-1 deficiency on the activation of B cells, naive B cells from $Egr1^{-/-}$mice and their wild-type (WT) littermates were activated to proliferate and differentiate, and then assayed by FACS. Proportions of cells undergoing proliferation and apoptosis did not differ between $Egr1^{-/-}$ and WT mice. However, $Egr1^{-/-}$ B cells gave rise to fewer plasma cells than WT B cells. Consistently, $Egr1^{-/-}$ mice produced significantly lower titer of antigen-specific IgG than their WT littermates upon immunization. Our results demonstrate that Egr-1 participates in the differentiation program of B cells into plasma cells, while it is dispensable for the proliferation and survival of mature B cells.

• IMMUNE NETWORK
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• v.12 no.6
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• pp.277-283
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• 2012

Vitamin C is an essential water-soluble nutrient which primarily exerts its effect on host defense mechanisms and immune homeostasis, but the mechanism related to immune-potentiation is poorly understood. Since dendritic cells (DCs) are known as a potent antigen presenting cell (APC) that could enhance the antigen specific immune responses, we investigate the effects of vitamin C on activation of DCs and its related mechanism by using dendritic cell lines, DC-1. First, we found that there was no damage on DC-1 by 2.5 mM of vitamin C. In the presence of vitamin C, the expression of CD80, CD86, and MHC molecules was increased, but it was decreased by the pre-treatment of SB203580, p38 MAPK-specific inhibitor. We confirmed the phosphorylation of p38 MAPK was increased by the treatment of vitamin C. Taken together, these results suggest that vitamin C could enhance the activity of dendritic cells via the up-regulation of the expression of CD80, CD86, and MHC molecules and the activation of p38 MAPK is related to this process.

• IMMUNE NETWORK
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• v.11 no.4
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• pp.210-215
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• 2011

It is already known that high concentration of vitamin C induces apoptosis on tumor cells. However, there is no report regarding the function of vitamin C on the modulation of immune susceptibility of cancer. Therefore, we investigated whether vitamin C can modulate immune susceptibility of tumor cells, especially on the induction of Fas-mediated apoptosis. First, the optimal concentration of vitamin C, which cannot induce damages on tumor cells for 36 hrs. We found that 2 mM of vitamin C did not show harmful effect. In addition, the optimal concentration of agonistic anti-Fas Abs for 18 hrs was examined. As a result, 400 ng/ml of agonistic anti-Fas Abs did not induce apoptosis on tumor cells. Next, we tried to find the effect of 2 mM of vitamin C on the modulation of the susceptibility to agonistic anti-Fas Abs. When tumor cells were cultured with 400 ng/ml of agonistic anti-Fas Abs for 18 hrs, after pre-treatment with 2 mM of vitamin C for 24 hrs, viability of cells was decreased. Interestingly, we found that the expression of Fas (CD95) and MHC class I was increased by the treatment of vitamin C. Taken together, vitamin C increases the susceptibility of tumor cells to anti-Fas Abs and the expression of Fas (CD95) and MHC class I on tumor cells.

• IMMUNE NETWORK
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• v.9 no.6
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• pp.236-242
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• 2009

Background: Melanoma is the most fatal form of skin cancer due to its rapid metastasis. Recently, several studies reported that selenium can induce apoptosis in melanoma cells. However, the precise mechanism remains to be elucidated. In this study, we investigated the effect of selenium on cell proliferation in murine melanoma and on tumor growth and metastasis in C57BL/6 mice. Methods: Cell proliferation was measured by MTT assay in selenium-treated melanoma cells. Cell cycle distribution was analysized by staining DNA with propidum iodide (PI). mRNA and protein expression related to cell cycle arrest was measured by reverse transcription PCR and western blot. Tumor growth and metastasis was measured by in vivo model. Results: Selenium was suppressed the proliferation of melanoma cells in a dose dependent manner. The growth inhibition of melanoma by selenium was associated with an arrest of cell cycle distribution at G0/G1 stage. The mRNA and protein level of CDK2/CDK4 was suppressed by treatment with selenium in a time-dependent manner. In vivo, tumor growth was not suppressed by selenium; however tumor metastasis was suppressed by selenium in mouse model. Conclusion: These results suggest that selenium might be a potent agent to inhibit proliferative activity of melanoma cells.

• IMMUNE NETWORK
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• v.13 no.2
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• pp.70-74
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• 2013

L-ascorbic acid (vitamin C) is one of the well-known antiviral agents, especially to influenza virus. Since the in vivo antiviral effect is still controversial, we investigated whether vitamin C could regulate influenza virus infection in vivo by using Gulo (-/-) mice, which cannot synthesize vitamin C like humans. First, we found that vitamin C-insufficient Gulo (-/-) mice expired within 1 week after intranasal inoculation of influenza virus (H3N2/Hongkong). Viral titers in the lung of vitamin C-insufficient Gulo (-/-) mice were definitely increased but production of anti-viral cytokine, interferon (IFN)-${\alpha}/{\beta}$, was decreased. On the contrary, the infiltration of inflammatory cells into the lung and production of pro-inflammatory cytokines, tumor necrosis factor (TNF)-${\alpha}$ and interleukin (IL)-${\alpha}/{\beta}$, were increased in the lung. Taken together, vitamin C shows in vivo antiviral immune responses at the early time of infection, especially against influenza virus, through increased production of IFN-${\alpha}/{\beta}$.