• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.311-320
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• 1999

Background: In recent years, tuberculosis has re-emerged as a major health problem in both industrialized & developing countries. Recent advances in identifying & purifying antigens secreted in active tuberculosis infection have lead to the development of serological assays based on a number of immunodominant antigens. To date, the most sensitive and specific of these antigens has been the 38-kDa antigen. Method: Two rapid membrane-based serologic assays using antigen(38-kDa) from mycobacterium tuberculosis for the diagnosis of tuberculosis were evaluated in 22 patients with smear-positive pulmonary tuberculosis, 14 patients with inactive pulmonary tuberculosis, and 9 patients with non-tuberculous lung disease. Result: The evaluation of validity(sensitivity, specificity, positive predictive value, negative predictive value, false positivity and false negativity) of STAT-PAK ULTRA FAST$^{(R)}$ were 77.3%, 28.6%, 63.0%, 44.4%, 71.4 %, and 22.7% for differential diagnosis of active pulmonary tuberculosis and inactive pulmonary tuberculosis, respectively. The evaluation of validity of STAT-PAK ULTRA FAST$^{(R)}$ were 77.3%, 33.3%, 73.9%, 37.5%, 66.7%, and 22.7% for differential diagnosis of active pulmonary tuberculosis and non-tuberculosis. The evaluation of validity of ICT Tuberculosis$^{(R)}$ were 54.5%, 57%, 66.7%, 44.4%, 42.9%, and 45.5% for differential diagnosis of active pulmonary tuberculosis and inactive pulmonary tuberculosis. The evaluation of validity of ICT Tuberculosis$^{(R)}$ were 54.5%, 100%, 100%, 47.4%, 0%, and 45.4% for differential diagnosis of active pulmonary tuberculosis and non-tuberculosis. Conclusion: We concluded no effectiveness of STAT-PAK ULTRA FAST$^{(R)}$ & ICT tuberculosis$^{(R)}$on serologic diagnosis of pulmonary tuberculosis. In the future, further large-scale study should be needed for serologic diagnosis of pulmonary tuberculosis.

• Journal of the Korean Chemical Society
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• v.58 no.4
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• pp.423-427
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• 2014

• 대한생식의학회:학술대회논문집
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• 2007.06a
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• pp.128-128
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• 2007

• Journal of Veterinary Science
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• v.24 no.1
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• pp.13.1-13.11
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• 2023

Background: Highly pathogenic avian influenza viruses (HPAIVs) is an extremely contagious and high mortality rates in chickens resulting in substantial economic impact on the poultry sector. Therefore, it is necessary to elucidate the pathogenic mechanism of HPAIV for infection control. Objective: Gene set enrichment analysis (GSEA) can effectively avoid the limitations of subjective screening for differential gene expression. Therefore, we performed GSEA to compare HPAI-infected resistant and susceptible Ri chicken lines. Methods: The Ri chickens Mx(A)/BF2(B21) were chosen as resistant, and the chickens Mx(G)/BF2(B13) were selected as susceptible by genotyping the Mx and BF2 genes. The tracheal tissues of HPAIV H5N1 infected chickens were collected for RNA sequencing followed by GSEA analysis to define gene subsets to elucidate the sequencing results. Results: We identified four differentially expressed pathways, which were immune-related pathways with a total of 78 genes. The expression levels of cytokines (IL-1β, IL-6, IL-12), chemokines (CCL4 and CCL5), type interferons and their receptors (IFN-β, IFNAR1, IFNAR2, and IFNGR1), Jak-STAT signaling pathway genes (STAT1, STAT2, and JAK1), MHC class I and II and their co-stimulatory molecules (CD80, CD86, CD40, DMB2, BLB2, and B2M), and interferon stimulated genes (EIF2AK2 and EIF2AK1) in resistant chickens were higher than those in susceptible chickens. Conclusions: Resistant Ri chickens exhibit a stronger antiviral response to HPAIV H5N1 compared with susceptible chickens. Our findings provide insights into the immune responses of genetically disparate chickens against HPAIV.

• Journal of Species Research
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• v.2 no.2
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• pp.127-144
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• 2013

An earthworm survey of Busan metropolitan area unearthed a dozen taxa in four families (including Enchytraeidae). Members of mostly common, cosmopolitan earthworm species-complexes were: Drawida cf. koreana Kobayashi, 1938, Amynthas cf. corticis (Kinberg, 1867), Aporrectodea trapezoides (Dug$\grave{e}$s, 1828) and Eisenia fetida (Savigny, 1826). Also found were Amynthas hupeiensis (Michaelsen, 1895), A. masatakae (Beddard, 1892) and Metaphire ryunome Blakemore, 2012 - the latter a new Korean record. New taxa are: moniligastrid Drawida songae yeongdo subsp. n.; megascolecid Amynthas carnosus roki subsp. n. which is compared to nominal taxon A. carnosus (Goto and Hatai, 1899) from Japan, to A. carnosus monstriferus (Kobayashi, 1936) stat. n. from Korea and to A. lichuanensis Wang and Qiu, 2005 stat. n. from China; plus lumbricid Eisenia japonica vaga subsp. n. deemed an objectively-based molecular taxon on its unique DNA COI gene barcode. Restoration of Eisenia xanthurus (Templeton, 1836) for E. andrei is mooted (in Appendix).

• Journal of Acupuncture Research
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• v.34 no.1
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• pp.1-9
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• 2017

Objectives : We investigated the synergistic effects of bee venom (BV) and natural killer (NK) cells on B16F10 melanoma cell apoptosis mediated by IL-4. Methods : We performed a cell viability assay to determine whether BV can enhance the inhibitory effect of NK-92MI cells on the growth of B16F10 melanoma cells, and western blot analysis to detect changes in the expression of IL-4, $IL-4R{\alpha}$, and other apoptosis-related proteins. EMSA was performed to observe the activity of STAT6. To confirm that the inhibitory effect of BV and NK cells was mediated by IL-4, the above tests were repeated after IL-4 silencing by siRNA (50 nM). Results : B16F10 melanoma cells co-cultured with NK-92MI cells and simultaneously treated by BV ($5{\mu}g/ml$) showed a higher degree of proliferation inhibition than when treated by BV ($5{\mu}g/ml$) alone or co-cultured with NK-92MI cells alone. Expression of IL-4, $IL-4R{\alpha}$, and that of other pro-apoptotic proteins was also enhanced after co-culture with NK-92MI cells and simultaneous treatment with BV ($5{\mu}g/ml$). Furthermore, the expression of anti-apoptotic bcl-2 decreased, and the activity of STAT6, as well as the expression of STAT6 and p-STAT6 were enhanced. IL-4 silencing siRNA (50 nM) in B16F10 cells, the effects of BV treatment and NK-92MI co-culture were reversed. Conclusion : These results suggest that BV could be an effective alternative therapy for malignant melanoma by enhancing the cytotoxic and apoptotic effect of NK cells through an IL-4-mediated pathway.

• BMB Reports
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• v.50 no.1
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• pp.25-30
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• 2017

In the central nervous system, viral infection can induce inflammation by up-regulating pro-inflammatory mediators that contribute to enhanced infiltration of immune cells into the central nervous areas. Celastrol is known to exert various regulatory functions, including anti-microbial activities. In this study, we investigated the regulatory effects and the mechanisms of action of celastrol against astrocytes activated with polyinosinic-polycytidylic acid (poly(I:C)), a synthetic dsRNA, as a model of pro-inflammatory mediated responses. Celastrol significantly inhibited poly(I:C)-induced expression of adhesion molecules, such as ICAM-1/VCAM-1, and chemokines, such as CCL2, CXCL8, and CXCL10, in CRT-MG human astroglioma cells. In addition, celastrol significantly suppressed poly(I:C)-induced activation of JNK MAPK and STAT1 signaling pathways. Furthermore, celastrol significantly suppressed poly(I:C)-induced activation of the $NF-{\kappa}B$ signaling pathway. These results suggest that celastrol may exert its regulatory activity by inhibiting poly(I:C)-induced expression of pro-inflammatory mediators by suppressing activation of JNK MAPK-STAT1/$NF-{\kappa}B$ in astrocytes.

• Molecules and Cells
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• v.38 no.2
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• pp.112-121
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• 2015

Ectopic expression of $14-3-3{\zeta}$ has been found in various malignancies, including lung cancer, liver cancer, head and neck squamous cell carcinoma (HNSCC), and so on. However, the effect of $14-3-3{\zeta}$ in the regulation of interactions between tumor cells and the immune system has not been previously reported. In this study, we aimed to investigate whether and how $14-3-3{\zeta}$ is implicated in tumor inflammation modulation and immune recognition evasion. In oral squamous cell carcinoma (OSCC) cell lines and cancer tissues, we found that $14-3-3{\zeta}$ is overexpressed. In OSCC cells, $14-3-3{\zeta}$ knockdown resulted in the up-regulated expression of inflammatory cytokines. In contrast, $14-3-3{\zeta}$ introduction attenuated cytokine expression in human normal keratinocytes and fibroblasts stimulated with interferon-${\gamma}$ (IFN-${\gamma}$) and lipopolysaccharide (LPS). Furthermore, supernatants from $14-3-3{\zeta}$ knockdown OSCC cells dramatically altered the response of peritoneal macrophages, dendritic cells and tumor-specific T cells. Interestingly, Stat3 was found to directly interact with $14-3-3{\zeta}$ and its disruption relieved the inhibition induced by $14-3-3{\zeta}$ in tumor inflammation. Taken together, our studies provide evidence that $14-3-3{\zeta}$ may regulate tumor inflammation and immune response through Stat3 signaling in OSCC.

• Natural Product Sciences
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• v.21 no.3
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• pp.205-209
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• 2015

Fucoidan, a sulfated polysaccharide is found in several types of edible brown algae. It has shown numerous biological activities; however, the molecular mechanisms on the activity against atopic dermatitis have not been reported yet. We now examined the effects of fucoidan on chemokine production co-induced by TNF-α/IFN-γ, and the possible mechanisms underlying these biological effects. Our data showed that fucoidan inhibited the TNF-α/IFN-γ-induced production of thymus and activation-regulated chemokine (TARC) and macrophagederived chemokine (MDC) mRNA in human keratinocytes HaCaT cells. Also, fucoidan suppressed phosphorylation of nuclear factor kappa B (NF-κB) and activation of signal transducer and activator of transcription (STAT)1 in a dose-dependent manner. In addition, fucoidan significantly inhibited activation of extracellular-signal-regulated kinases (ERK) phosphorylation. These data indicate that fucoidan shows anti-inflammatory effects by suppressing the expression of TNF-α/IFN-γ-induced chemokines by blocking NF-κB, STAT1, and ERK1/2 activation, suggestive of as used as a therapeutic application in inflammatory skin diseases, such as atopic dermatitis.

• Archives of Pharmacal Research
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• v.28 no.4
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• pp.451-457
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• 2005

Experimental studies have demonstrated that the triple combination of amantadine (A)/ ursodeoxycholic acid (UDCA, U)/ biphenyl dimethyl dicarboxylate (DDB, D) might have a preferential antiviral effect compared with that observed in interferon-induced antiviral signal pathways, such as those of $STAT1\alpha$ and the 6-16 genes. To confirm the results, this study examined whether th signal transduction for the antiviral activity in HepG2 2.2.15 was induced dependently or independently of interferon. To accomplish this, the correlation between the $STAT1\alpha$ and 6-16 genes, and nitric oxide, for the mediation of the antiviral activity was assessed. The increase in nitric oxide in the UDCA groups suggests that the inhibition of viral gene replication was enhanced by the amantadine combinations (AU and AUD), and might be more effective if incubated for longer periods. It was found that $STAT1\alpha$ was activated by the amantadine combination, although to a lesser extent than that of $interferon-\alpha$, and the primary endpoints examined for the inhibition of gene expression (HBsAg and HBcAg) were remarkably well regulated. This suggests that the amantadine triple, or at least the double, combination had better clinical benefits than those of $IFN-\alpha$ and the nucleoside analogue single treatment. This demonstrates that the amantadine combination might be a substitute for the existing HBV therapy if the results of in vivo and in vitro studies concur.