• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.20 no.1 s.32
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• pp.99-114
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• 2007

Objectives : Atopic dermatitis has a close relationship with damage of skin barrier function. To investigate the effects of Bangpungtongsungsan(BT) extract to the skin damage on mice model after atopic dermatitis elicitation, this study was done through forcing injury to mice's skin. Methods : The BALB/c mice were distributed into three groups: control(CON) group, atopic dermatitis(AD)-elicited group, Bangpungtongsungsan(BT)-treated group. AD-elicited and BT-treated group were caused AD according to the method of Christophers E., Mrowietz and Minehiro. The BT extract was administered for 48 hours to BT-treated group. We observed changes of external dermal formation, eosinophils in vasculature, lipid formation in stratum corneum, distribution of ceramide, distribution of capillary, $I{\kappa}B$ kinase(IKK) and induce nitric oxide synthase(iNOS) mRNA expression. We used the statistical methods of student t-test(p<0.05). Results : After dispensing BT extract into the AD-elicited group, the number of eosinophil as an atopic index in mice noticeably decreased and dermal injury decreased. Also the decrease of hyperplasia, degranulated mast cells, angiogenesis and substance P were shown. The lipid lamellae, lipid protect formation, were repaired and the distribution of ceramide which inhibit protein kinase C(PKC) activation increased, and the PKC caused inhibition of nuclear $factor(NF)-{\kappa}B$ activation. As a result of inhibition of $NF-{\kappa}B$ activation, iNOS production were inhibited and apoptotic cell were increased. Moreover the decrease of IKK and iNOS mRNA expression in BT-treated RAW 264.7 cell were noted. Conclusion : BT mitigated skin damage on mice model after atopic dermatitis elicitation through recovering skin barrier function and inhibiting nuclear $factor(NF)-{\kappa}B$ activation.

• The Korean Journal of Pain
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• v.34 no.1
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• pp.47-57
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• 2021

Background: Lumbar disc herniation (LDH) is a common cause of radicular pain, but the mechanism is not clear. In this study, we investigated the engagement of toll-like receptor 4 (TLR4) and the nuclear factor-kappa B (NF-κB) in radicular pain and its possible mechanisms. Methods: An LDH model was induced by autologous nucleus pulposus (NP) implantation, which was obtained from coccygeal vertebra, then relocated in the lumbar 4/5 spinal nerve roots of rats. Mechanical and thermal pain behaviors were assessed by using von Frey filaments and hotplate test respectively. The protein level of TLR4 and phosphorylated-p65 (p-p65) was evaluated by western blotting analysis and immunofluorescence staining. Spinal microglia activation was evaluated by immunofluorescence staining of specific relevant markers. The expression of proand anti-inflammatory cytokines in the spinal dorsal horn was measured by enzyme linked immunosorbent assay. Results: Spinal expression of TLR4 and p-NF-κB (p-p65) was significantly increased after NP implantation, lasting up to 14 days. TLR4 was mainly expressed in spinal microglia, but not astrocytes or neurons. TLR4 antagonist TAK242 decreased spinal expression of p-p65. TAK242 or NF-κB inhibitor pyrrolidinedithiocarbamic acid alleviated mechanical and thermal pain behaviors, inhibited spinal microglia activation, moderated spinal inflammatory response manifested by decreasing interleukin (IL)-1β, IL-6, tumor necrosis factor-α expression and increasing IL-10 expression in the spinal dorsal horn. Conclusions: The study revealed that TLR4/NF-κB pathway participated in radicular pain by encouraging spinal microglia activation and inflammatory response.

• Microbiology and Biotechnology Letters
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• v.32 no.2
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• pp.190-194
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• 2004

The gene product of dctD (DctD) activates transcription from the dctA promoter regulatory region by the $\sigma^{54}$ -holoenzyme form ofRNA polymerase ($E\sigma^{54}$ ) in Rhizobium meliloti and R. leguminosarum. The Escherichia coli integration host factor (IHF) stimulated DctD-mediated activation from the dctA promoter regulatory region of R. leguminosarum but not R. meliloti. In the absence of UAS, IHF inhibited DctD-mediated activation from both of these promoter regulatory regions. IHF also inhibited activation from R. leguminosarum dctA by nitrogen regulatory protein C (NtrC), another activator of $E\sigma^{54}$ but not by one which lacks a specific binding site in this promoter regulatory region. IHF, however, stimulated NtrC-mediated activation from the R. meliloti dctA promoter. Upon removal of the UAS, IHF inhibited NtrC-mediated transcription activation from the R. meliloti dctA promoter regulatory region. These data suggest that IHF likely faciliates productive contacts between the activators NtrC or DctD and $E\sigma^{54}$ to stimulate activation from dctA promoter.

• International Journal of Internet, Broadcasting and Communication
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• v.14 no.1
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• pp.136-141
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• 2022

A very complex task in deep learning such as image classification must be solved with the help of neural networks and activation functions. The backpropagation algorithm advances backward from the output layer towards the input layer, the gradients often get smaller and smaller and approach zero which eventually leaves the weights of the initial or lower layers nearly unchanged, as a result, the gradient descent never converges to the optimum. We propose a two-factor non-saturating activation functions known as Bea-Mish for machine learning applications in deep neural networks. Our method uses two factors, beta (𝛽) and alpha (𝛼), to normalize the area below the boundary in the Mish activation function and we regard these elements as Bea. Bea-Mish provide a clear understanding of the behaviors and conditions governing this regularization term can lead to a more principled approach for constructing better performing activation functions. We evaluate Bea-Mish results against Mish and Swish activation functions in various models and data sets. Empirical results show that our approach (Bea-Mish) outperforms native Mish using SqueezeNet backbone with an average precision (AP50val) of 2.51% in CIFAR-10 and top-1accuracy in ResNet-50 on ImageNet-1k. shows an improvement of 1.20%.

• Molecules and Cells
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• v.40 no.10
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• pp.706-713
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• 2017

Osteoclasts are bone-resorbing cells that are derived from hematopoietic precursor cells and require macrophage-colony stimulating factor and receptor activator of nuclear factor-${\kappa}B$ ligand (RANKL) for their survival, proliferation, differentiation, and activation. The binding of RANKL to its receptor RANK triggers osteoclast precursors to differentiate into osteoclasts. This process depends on RANKL-RANK signaling, which is temporally regulated by various adaptor proteins and kinases. Here we summarize the current understanding of the mechanisms that regulate RANK signaling during osteoclastogenesis. In the early stage, RANK signaling is mediated by recruiting adaptor molecules such as tumor necrosis factor receptorassociated factor 6 (TRAF6), which leads to the activation of mitogen-activated protein kinases (MAPKs), and the transcription factors nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and activator protein-1 (AP-1). Activated NF-${\kappa}B$ induces the nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), which is the key osteoclastogenesis regulator. In the intermediate stage of signaling, the co-stimulatory signal induces $Ca^{2+}$ oscillation via activated phospholipase $C{\gamma}2$ ($PLC{\gamma}2$) together with c-Fos/AP-1, wherein $Ca^{2+}$ signaling facilitates the robust production of NFATc1. In the late stage of osteoclastogenesis, NFATc1 translocates into the nucleus where it induces numerous osteoclast-specific target genes that are responsible for cell fusion and function.

• The Journal of Korean Obstetrics and Gynecology
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• v.21 no.1
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• pp.39-54
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• 2008

Purpose: The purpose of this study was to investigate the anti-inflammatory effects of the water extract of Omisodokeum (OMSDE) on peritoneal macrophages, Methods: To verify the anti-inflammatory mechanism of OMSDE, the activation of nuclear $factor-{\kappa}B$ $(NF-{\kappa}B)$ and the phosphorylation of MAPK were examined. Results: The extract of OMSDE suppressed the production of LPS-induced nitric oxide (NO), tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$, IL-6 and IL-12 in the macrophages. OMSDE inhibited the degradation of inhibitory ${\kappa}B-{\alpha}$ $(I{\kappa}B-{\alpha})$ and it suppressed the activation of extracellular signal-regulated kinase (ERK 1/2) but didn't inhibit c-Jun N-terminal kinase (JNK) and p38, indicating that OMSDE may inhibit the pro-inflammatory cytokine production process by inhibiting the activation of $NF-{\kappa}B$ and ERK 1/2. Furthermore, OMSDE inhibited the production of interferon $(IFN)-{\beta}$ but didn't inhibit of $IFN-{\alpha}$ in the LPS-stimulated macrophages through the down-regulation of interferon regulatory factor (IRF)-1 and IRF-7. The Oral administration of OMSDE inhibited LPS-induced endotoxin shock and the production of $TNF-{\alpha}$ in serum but didn't inhibit of $IL-1{\beta}$ and IL-6. Conclusion: These results suggest that OMSDE may be effective in the prevention and treatment of inflammatory diseases.

• The Journal of the Korea Contents Association
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• v.16 no.4
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• pp.594-603
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• 2016

This study analyzed that introduction function and program how influence about quality of life local resident and development of region according to real development. Also, it suggested policy implications of area activation plan through complex development of railway station area. In research method, the factor and structure affecting area activation in complex development of railway station area analyzed positively using the PLS structural equation focused on citizen near station area. As a result of study, in regional economic vitalization, the factors of software(marketing support, transfer system support, plan and design support, complex development support, law institution improvement, etc) and the factors of hardware(traffic function, information exchange function, commercial business function, housing features, amenity function, etc) are represented to influence significantly and then, in quality of life of local resident, the factor of hardware analyzed to influence significantly, but the factor of software and network did not. In comparison, the factor of network is represented that it did not contributed in regional economic vitalization and quality of life of local resident. So, political supplementations are needed.

• Natural Product Sciences
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• v.24 no.1
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• pp.13-20
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• 2018

Estragole is a naturally occurring phenylpropanoid obtained from essential oils found in a broad diversity of plants. Although the phenylpropanoids show many biological activities, clear regulation of the inflammatory signaling pathways has not yet been determined. Here, we scrutinized the anti-inflammatory effect of estragole. The anti-inflammatory effect of estragole was determined through the inhibitory mechanisms of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), nuclear factor kappa B ($NF-{\kappa}B$), and mitogen-activated protein kinases (MAPK) pathways and the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2)/heme oxygenase (HO)-1 pathways in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Estragole significantly inhibited NO production, iNOS and COX-2 expression as well as LPS-induced $NF-{\kappa}B$ and MAPK activation. Furthermore, estragole suppressed LPS-induced intracellular ROS production but up-regulated the stress response gene HO-1 via the activation of transcription factor Nrf-2. These findings demonstrate that estragole inhibits the LPS-induced expression of inflammatory mediators via the down-regulation of iNOS, COX-2, $NF-{\kappa}B$, and MAPK pathways, as well as the up-regulation of the Nrf-2/HO-1 pathway, indicating that this phenylpropanoid has potential therapeutic and preventive applications in various inflammatory diseases.

• Molecules and Cells
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• v.21 no.2
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• pp.237-243
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• 2006

Brain-derived neurotrophic factor (BDNF) is a neuromodulator of nociceptive responses in the dorsal root ganglia (DRG) and spinal cord. BDNF synthesis increases in response to nerve growth factor (NGF) in trkA-expressing small and medium-sized DRG neurons after inflammation. Previously we demonstrated differential activation of multiple BDNF promoters in the DRG following peripheral nerve injury and inflammation. Using reporter constructs containing individual promoter regions, we investigated the effect of NGF on the multiple BDNF promoters, and the signaling pathway by which NGF activates these promoters in PC12 cells. Although all the promoters were activated 2.4-7.1-fold by NGF treatment, promoter IV gave the greatest induction. The p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, phosphatidylinositol 3-kinase (PI-3K) inhibitor, LY294003, protein kinase A (PKA) inhibitor, H89, and protein kinase C (PKC) inhibitor, chelerythrine, had no effect on activation of promoter IV by NGF. However, activation was completely abolished by the MAPK kinase (MEK) inhibitors, U0126 and PD98059. In addition, these inhibitors blocked NGF-induced phosphorylation of extracellular signal-regulated protein kinase (ERK) 1/2. Taken together, these results suggest that the ERK1/2 pathway activates BDNF promoter IV in response to NGF independently of NGF-activated signaling pathways involving PKA and PKC.

• The Journal of Internal Korean Medicine
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• v.35 no.3
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• pp.262-273
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• 2014

Objectives: This study was carried out to investigate the protective effect of Coptidis Rhizoma steamed with rice wine (CR) against gastroduodenal mucosal injury through inhibiting inducible nitric oxide synthase (iNOS) activation. Methods: In in vitro experiment, LPS-induced RAW 264.7 macrophages were treated with CR(0.4, 0.6, 0.8, 1.0 mg/ml) and iNOS mRNA expression and nitric oxide (NO) production were measured. In in vivo experiment normal group mice were treated with neither ethanol nor CR. Both control and sample group mice were orally administrated with ethanol. Five hours after ethanol administration control group mice were orally administrated with distilled water, sample group mice were orally administrated with CR. After three days administration, gastroduodenal mucosa of mice was observed histopathologically and iNOS, nuclear factor-kappa B (NF-${\kappa}B$) activation were observed immunohistochemically. Results: In in vitro experiment iNOS mRNA expression and NO production in LPS-induced RAW 264.7 macrophages were decreased by CR dose-dependently. In in vivo experiment, gastroduodenal mucosal injury was repaired by CR and iNOS, NF-${\kappa}B$ activation in gastroduodenal mucosa were decreased by CR. Conclusions: Coptidis Rhizoma steamed with rice wine has a protective effect against gastroduodenal mucosal injury through inhibiting iNOS activation.