• BMB Reports
• /
• 제54권8호
• /
• pp.425-430
• /
• 2021

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) induces coronavirus disease 2019 (COVID-19) and may increase the risk of adverse outcomes in lung cancer patients. In this study, we investigated the expression and function of mucin 1 (MUC1) after SARS-CoV-2 infection in the lung epithelial cancer cell line Calu-3. MUC1 is a major constituent of the mucus layer in the respiratory tract and contributes to pathogen defense. SARS-CoV-2 infection induced MUC1 C-terminal subunit (MUC1-C) expression in a STAT3 activation-dependent manner. Inhibition of MUC1-C signaling increased apoptosis-related protein levels and reduced proliferation-related protein levels; however, SARS-CoV-2 replication was not affected. Together, these results suggest that increased MUC1-C expression in response to SARS-CoV-2 infection may trigger the growth of lung cancer cells, and COVID-19 may be a risk factor for lung cancer patients.

• Journal of Microbiology and Biotechnology
• /
• 제15권3호
• /
• pp.626-632
• /
• 2005

A new bacterium BL-2 excreting a novel cationic polyglucosamine biopolymer was isolated from the spoiled leaves of Chinese cabbage and identified as Enterobacter sp. BL-2. The isolated Enterobacter sp. BL-2 was cultivated in pH-stat fed-batch culture using acetic acid as the feeding stock at pH 8.0, resulting in 17.11 g/l of cells and 1.53 g/l of an extracellular biopolymer after 72 h. The excreted biopolymer was purified by a three-step procedure, involving ethanol precipitation and deproteinizations, to a nearly homogeneous state, and its molecular weight was found to be 106 kDa. It was composed of glucosamine, rhamnose, and galactose at a molar ratio of 86.4:1.6:1.0, respectively, indicating a rarely found novel high-glucosamine-containing biopolymer. The FT-IR and $^{13}C-NMR$ spectra of the novel cationic polyglucosamine biopolymer PGB-l revealed a close identity with chitosan from crab shell. It can effectively flocculate various suspended solids, including kaolin clay, $Ca(OH)_2,\;Al_{2}O_3$, active carbon, microbial cells, and acidic dyes.

• Animal cells and systems
• /
• 제2권1호
• /
• pp.117-122
• /
• 1998

D-raf, a Drosophila homolog of the human c-raf-1, is known as a signal transducer in cell proliferation and differentiation. A previous study found that the D-raf gene expression is regulated by the DNA replication-related element (DRE)/DRE-binding factor (DREF) system. In this study, we found the sequences homologous to transcription factor C/EBP, MyoD, STAT and Myc recognition sites in the D-raf promoter. We have generated various base substitutional mutations in these recognition sites and subsequently examined their effects on D-raf promoter activity through transient CAT assays in Kc cells with reporter plasmids p5'-878DrafCAT carrying the mutations in these binding sites. Through gel mobility shift assay using nuclear extracts of Kc cells, we detected factors binding to these recognition sites. Our results show that transcription factor C/EBP, STAT and Myc binding sites in D-raf promoter region play a positive role in transcriptional regulation of the D-raf gene and the Myo D binding site plays a negative role.

• 응용통계연구
• /
• 제11권2호
• /
• pp.389-401
• /
• 1998

본 논문에서는 멀티미디어를 활용한 회귀분석 학습시스템 CybeRClass(Cyber Regression Class)를 소개하고자 한다. CybeRClass는 음성정보와 애니메이션 등을 활용하여 회귀분석에 대한 학습을 시켜주는 시스템이다. 이 시스템은 군집분석이나 판별분석 등의 다변량분석 학습이 가능하도록 설계되었다. 멀티미디어 기술을 위한 도구로는 Multimedia ToolBook을 사용하였으며, 통계계산과 통계그라픽을 위해서는 객체지향 통계 언어인 Xlisp-Stat을 사용하였다.

• 대한한방부인과학회지
• /
• 제26권2호
• /
• pp.17-32
• /
• 2013

Objectives: The purpose of this study was to investigate whether Lonicera japonica(LJ) could inhibit LPS-induced type I IFN production. Methods: To evaluate inhibitory effect of LJ on type I IFN, we examined type I IFN, IRF-1, 7 and IL-10 production on LPS-induced macrophages using real time RT-PCR. Next, we observed the interaction of type I IFN, IRF-1, 7 and IL-10 using IL-10 neutralizing antibody. Finally we examined the activation of STAT-1, 3 using western blot. Results: LJ inhibited Type I IFN expression of mRNA and increased IL-10 expression of mRNA. Also LJ inhibited the level of IRF-1, 7 mRNA and the nuclear translocation of IRF-3. Further more, LJ reduced the activation of STAT-1, 3 which are involved in continuous secretion of immune cytokines. Blockade of IL-10 action caused a significant reduction of type I IFN and IRF-1, 7 than LPS-induced LJ pretreatment. Conclusions: LJ inhibits LPS-induced production of type I IFN by IL-10. This study may provide a clinical basis for anti-inflammatory properties of LJ.

• Asian Pacific Journal of Cancer Prevention
• /
• 제16권12호
• /
• pp.5069-5073
• /
• 2015

The single nucleotide polymorphism (SNP) rs1053004 in Signal transducer and activator of transcription 3 (STAT3) was recently reported to be associated with chronic hepatitis B (CHB)-related hepatocellular carcinoma (HCC) in a Chinese cohort. This study was aimed at investigating whether the SNP might also contribute to HCC susceptibility in the Thai population. Study subjects were enrolled and divided into 3 groups including CHB-related HCC (n=211), CHB without HCC (n=233) and healthy controls (n=206). The SNP was genotyped using allelic discrimination assays based on TaqMan real-time PCR. Data analysis revealed that the distribution of different genotypes was in Hardy-Weinberg equilibrium (P>0.05). The frequencies of allele T (major allele) in HCC patients, CHB patients and healthy controls were 51.4%, 58.6% and 61.4%, respectively, whereas the frequencies of C allele (minor allele) were 48.6%, 41.4% and 38.6%. The C allele frequency was higher in HCC when compared with CHB patients (odds ratio (OR)=1.34, 95% confidence interval (CI)=1.02-1.74, P=0.032). The genotype of SNP rs1053004 (CC versus TT+TC) was significantly associated with an increased risk when compared with CHB patients (OR=1.83, 95% CI=1.13-2.99, P=0.015). In addition, we observed a similar trend of association when comparing HCC patients with healthy controls (OR=1.77, 95% CI=1.07-2.93, P=0.025) and all controls (OR=1.81, 95% CI=1.19-2.74, P=0.005). These findings suggest that the SNP rs1053004 in STAT3 might contribute to HCC susceptibility and could be used as a genetic marker for HCC in the Thai population.

• 한국식품영양과학회지
• /
• 제36권1호
• /
• pp.32-42
• /
• 2007

본 연구의 목적은 DSS로 유발시킨 대장염 동물모델에서 생식섭취가 장관 내 면역조절에 미치는 영향에 대하여 검토해보고자 했다. 그 결과, 생식섭취가 DSS로 유발시킨 대장염에서 normal군보다 IFN-$\gamma$의 함량을 증가시키고, IL-4와 IL-10의 함량은 감소시킴이 관찰되었다. 또한, 증가된 Th1 세포의 cytokine과 감소된 Th2 세포의 cytokine은 염증이 유발된 후, 생식을 통한 치료로써 변환시킬 수 있음을 증명하였다. 이러한 연구 결과를 볼 때 DSS로 유발시킨 대장염에서 생식 섭취를 통한 치료는 IL-4와 IL-10과 같은 염증성 cytokine의 억제기능을 통하여 면역시스템을 강화시키고, 손상된 염증을 완화시켜 줄 것으로 판단된다. 생식의 면역조절에 관한 자세한 기전은 아직 밝혀져 있지 않지만, 염증성 장질환에서 생식섭취가 면역학적 역할에 대한 새로운 양상들에 대한 연구가 더욱더 필요할 것으로 사료된다.

• International Journal of Reliability and Applications
• /
• 제12권2호
• /
• pp.103-116
• /
• 2011

A series-parallel system with independent but non-identical components is considered. The expressions have been derived for the joint reliability importance (JRI) of m (${\geq}2$) components, chosen from a series-parallel system. JRIs of components of two different series-parallel systems are studied analytically and graphically.

• Journal of Applied Biological Chemistry
• /
• 제64권2호
• /
• pp.185-192
• /
• 2021

건선(Psoriasis)은 IL-6, CXCL8, TNF-α 및 IFN-γ뿐만 아니라 Th17 세포에서 분비되는 IL-17A 등 다양한 염증성 사이토카인에 의해 표피의 과증식(hyperkeratosis) 및 만성적 염증(inflammation)이 유발되는 난치성 피부 질환이다. 소목(Caesalpinia sappan L.)의 유효성분으로 알려진 브라질린(brazilin)은 항산화, 항염증 및 피부 장벽 개선 등의 효능이 알려졌다. 특히, tumor necrosis factor (TNF)-α 자극 HaCaT 각질형성세포 모델에서 브라질린의 건선 치료 소재 가능성을 보여주었다. 그러나, 직접적인 건선 유발 인자인 C-C motif chemokine ligand (CCL) 20의 조절은 전혀 보고되지 않았다. 따라서, 본 연구에서는 건선 유사 모델을 활용해 CCL20 발현 조절 여부 및 그 기작에 대해 규명하고자 하였다. IL-17A로 자극된 HaCaT 세포에서 브라질린은 CCL20, CXCL8 발현 및 signal transducer and transcription (STAT)3 인산화를 유의하게 억제하였다. 또한, 브라질린은 TNF-α/IL-17A/IFN-γ 3종 사이토카인으로 처리된 조건에서도 STAT3 인산화를 억제하며 염증성 분자(CXCL8, CCL20, IL-1, IL-6, 및 TNF-α)의 발현을 하향 조절하였다. 마지막으로 브라질린은 TNF-α/IL-17A/IFN-γ로 자극된 건선 유사 환경에서 피부 장벽 개선에도 유의적인 영향을 미쳤다. 위 결과들을 통해 우리는 궁극적으로 브라질린이 STAT3 인산화 억제를 통해 CCL20 발현을 하향 조절하며, 건선 유발 사이토카인들의 발현 또한 억제함을 알 수 있었다. 향후, 건선 동물모델 및 임상시험을 통해 브라질린의 건선 개선에 대한 효능이 검증된다면, 건선 환자에게 잠재적인 치료 물질로 사용될 수 있을 것으로 기대된다.

• BMB Reports
• /
• 제33권6호
• /
• pp.454-462
• /
• 2000

Interleukin-4(IL-4) is known to be a major cytokine regulating immunoglobulin E(IgE) response by the induction of IgE production and type II IgE receptor(IgER II: CD23) expression. Recently, however, the role of neuroendocrine factors has been implicated in modulating the IgE response. Among various neuroendocrine growth factors, we investigated the effects of the insulin-like growth factor-1(IGF-1) since IL-4 and IGF-1 share common intracellular signaling molecules, such as the insulin receptor substrate-1/2(IRS-1/2) to induce a specific cellular response. In the human peripheral blood mononuclear cell (PBMC) cultures, IGF-1 was capable of inducing a substantial level of IgE production in a dose-dependent manner. It also noticeably upregulated the IL-4-induced or IL-4 plus anti-CD40-induced IgE production. Similarly, the IGF-1-induced IgE production was enhanced by IL-4 or anti-CD40 in an additive manner, which became saturated at high concentrations of IGF-1. Although IGF-1 alone did not induce IgER II (CD23) expression, it augmented the IL-4-induced surface CD23 expression in a manner similar to the action of anti-CD40. These results imply that IGF-1 is likely to utilize common signaling pathways with IL-4 and anti-CD40 to induce IgE and IgER II expression. In support of this notion, we observed that IGF-1 enhanced the IL-4-induced signal transducers and activators of transcription 6(STAT6) activation and independently induced $NF-{\kappa}B$ activation. Both of these bind to the IgE(C) or IgER II (CD23) promoters. Together, our data suggest that IL-4 and IGF-1 work cooperatively to activate STAT6 and $NF-{\kappa}B$. This leads to the subsequent binding of these transcription factors to the $C{\varepsilon}$ and CD23 promoters to enhance the expression of IgE and IgER II. The observed differential ability of IGF-1 on the induction of IgE vs. IgER II is discussed based on the different structure of the two promoters.