• Journal of Microbiology and Biotechnology
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• v.11 no.1
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• pp.56-60
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• 2001

A kerosene fungus of Cladosporium resinae NK-1 was examined for its ability to degrade individual n-alkanes and aromatic hydrocarbons by gas chromatography-mass spectrometry, and its organic solvent-tolerance was investigated by making use of the water-organic solvent suspension culture method. It grew on a wide range of solvents of varying hydrophobicities and it was found to have tolerance to various kinds of toxic organic solvents (10%, v/v) such as n-alkanes, cyclohexane, xylene, styrene, and toluene. A hydrocarbon degradation experiment indicated that NK-1 had a greater n-alkane degrading ability compared to that of the other selected strains. C. resinae NK-1, which could utilize 8-16 carbon chain-length n-alkanes of medium chain-length as a carbon source, could not assimilate the shorter chain-length n-alkanes and aromatic hydrocarbons tested so far. The n-alkane degrading enzyme activity was found in the mycelial extract of the organism.

• Journal of the Korean Mathematical Society
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• v.43 no.4
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• pp.815-828
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• 2006

Let {$V_{nk},\;k\;{\geq}\;1,\;{\geq}\;1$} be an array of rowwise independent random elements which are stochastically dominated by a random variable X with $E\|X\|^{\frac{\alpha}{\gamma}+{\theta}}log^{\rho}(\|X\|)\;<\;{\infty}$ for some ${\rho}\;>\;0,\;{\alpha}\;>\;0,\;{\gamma}\;>\;0,\;{\theta}\;>\;0$ such that ${\theta}+{\alpha}/{\gamma}<2$. Let {$a_{nk},k{\geq}1,n{\geq}1$) be an array of suitable constants. A complete convergence result is obtained for the weighted sums of the form $\sum{^\infty_k_=_1}\;a_{nk}V_{nk}$.

• Korean Journal of Head & Neck Oncology
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• v.36 no.2
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• pp.45-50
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• 2020

Extranodal Natural Killer (NK)/T-cell lymphoma, nasal type, is a subtype of non-Hodgkin lymphoma, strongly associated with Epstein-Barr virus. Extranodal NK/T-cell lymphoma mostly affects the nasal cavity and there has been no report of the disease's occurrence at the base of tongue. Here we report a case of 43-year-old man who presented with a diffuse ulcerative lesion at the base of tongue. Because the patient had oral bleeding, tracheostomy and lingual artery ligation was performed via a transcervical approach to control bleeding and protect the upper airway. We performed a deep biopsy through the lateral pharyngotomy approach, and finally, the patient was diagnosed with extranodal NK/T-cell lymphoma, nasal type. We report this rare case of extranodal NK/T cell lymphoma at the base of tongue with a literature review.

• Journal of Acupuncture Research
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• v.31 no.1
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• pp.111-119
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• 2014

Objectives : I investigated whether Bee Venom can synergistically strengthen the cytotoxic effects of NK-92 cells, enhancing the inhibition of the growth of Lung Cancer Cells including A549 and NCI-H460 through induction of death receptor dependent extrinsic apoptosis and NO generation in the Nitro-oxide pathway. Methods : Bee Venom inhibited cell proliferation of A549 or NCI-H460 Human Lung Cancer Cells as well as NK-92 Cells. Moreover, when they were co-punctured with NK cells and concomitantly treated by 3 ${\mu}g/ml$ of Bee Venom, more influence was exerted on inhibition of proliferation of A549 or NCI-H460 Human Lung Cancer Cells than BV or NK cell co-culture alone. Results : The expression of Fas, TNFR2, DR3, DR6 in A549 Lung Cancer Cells was significantly increased by co-culture of NK-92 cells and treatment of 3 ${\mu}g/ml$ of Bee Venom, compared to co-culture of NK-92 cells alone, whereas the expression of Fas, TNFR2, DR6 in NCI-H460 Lung Cancer Cells was significantly increased by co-culture of NK-92 cells, representing no synergistic effects in the co-culture of NK-92 cell and concomitant treatment of 3 ${\mu}g/ml$ of Bee Venom. Coincidently, caspase-8, a expression of pro-apoptotic proteins in the extrinsic apoptosis pathway demonstrated same results as the above. Meanwhile, In NO generation, there is little change of NO generation in co-culture of NK-92 cells with A549 cells as well as the co-culture of NK-92 cell with them and concomitant treatment of 3 ${\mu}g/ml$ of Bee Venom, whereas increase of NO generation was shown in co-culture of NK-92 cells with NCI-H460 cells as well as the co-culture of NK-92 cell with them and concomitant treatment of 3 ${\mu}g/ml$ of Bee Venom, although synergistic effects by Bee Venom was not found. Conclusions : These present data provide that Bee Venom could be useful candidate compounds to enhance lung cancer growth inhibiting ability of NK-92 cells through DR expression and the related apoptosis.

• 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.

• Molecules and Cells
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• v.47 no.3
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• pp.100007.1-100007.11
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• 2024

Recent evidence establishes a pivotal role for obesity-induced inflammation in precipitating insulin resistance and type-2 diabetes. Central to this process is the proinflammatory M1 adipose-tissue macrophages (ATMs) in epididymal white adipose tissue (eWAT). Notably, natural killer (NK) cells are a crucial regulator of ATMs since their cytokines induce ATM recruitment and M1 polarization. The importance of NK cells is shown by the strong increase in NK-cell numbers in eWAT, and by studies showing that removing and expanding NK cells respectively improve and worsen obesity-induced insulin resistance. It has been suggested that NK cells are activated by unknown ligands on obesity-stressed adipocytes that bind to NKp46 (encoded by Ncr1), which is an activating NK-cell receptor. This was supported by a study showing that NKp46-knockout mice have improved obesity-induced inflammation/insulin resistance. We therefore planned to use the NKp46-knockout mice to further elucidate the molecular mechanism by which NKp46 mediates eWAT NK-cell activation in obesity. We confirmed that obesity increased eWAT NKp46⁺ NK-cell numbers and NKp46 expression in wild-type mice and that NKp46-knockout ablated these responses. Unexpectedly, however, NKp46-knockout mice demonstrated insulin resistance similar to wild-type mice, as shown by fasting blood glucose/insulin levels and glucose/insulin tolerance tests. Obesityinduced increases in eWAT ATM numbers and proinflammatory gene expression were also similar. Thus, contrary to previously published results, NKp46 does not regulate obesity-induced insulin resistance. It is therefore unclear whether NKp46 participates in the development of obesity-induced inflammation and insulin resistance. This should be considered when elucidating the obesity-mediated molecular mechanisms that activate NK cells.

• Korean Journal of Veterinary Research
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• v.43 no.3
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• pp.405-414
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• 2003

The purpose of this study was to assess the role of tachykinins (TK) in mediating nonadrenergic noncholinergic (NANC) contractions produced by electrical field stimulation (EFS) in the longitudinal muscle of the rat ileum. In the presence of atropine ($1{\mu}M$), guanethidine ($5{\mu}M$), and L-nitroarginine (L-NNA, $200{\mu}M$), EFS (0.5ms pulse duration, 120 V, 1-20 Hz for 2 min) produced a frequency-dependent slowly-developing tonic contraction with superimposed phasic contractions ('on'-contraction) followed by off slowly-decreasing tonic and superimposed phasic contractions ('off'-contraction) of mucosa-free longitudinal oriented muscle strip. These EFS induced responses were blocked by tetrotoxin. $NK_1$ receptor selective antagonist L-732,138 strongly inhibited the EFS-induced excitatory responses. However $NK_2$ receptor selective antagonist, GR 159897 and $NK_3$ receptor selective antagonist SB 222200 did not significantly inhibited the responses. $NK_1$ receptor selective agonist [$Sar^9$,$Met(O_2)^{11}$] Substance P and $NK_2$ receptor selective agonist [${\beta}-Ala^8$]-neurokinin A (4-10) induced tonic contraction with superimposed phasic contractions of longitudinal oriented muscle strip and almost blocked by selective antagonist L-732,138 and GR 159897, respectively. But $NK_3$ receptor selective agonist senktide did not showed any effect. Nifedipine ($1{\mu}M$) abolished the contraction produced either by EFS or by the TK receptor agonists [$Sar^9$,$Met(O_2)^{11}$] Substance P or [${\beta}-Ala^8$]-neurokinin A (4-10). It is concluded that, in the longitudinal muscle of rat ileum, both $NK_1$ and $NK_2$ receptors modulated the responses to exogenous tachykinins, whereas $NK_1$ is mainly involved in NANC neuromuscular contraction.

• Bulletin of the Korean Mathematical Society
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• v.37 no.2
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• pp.255-263
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• 2000

Let ${X_{nk}}, u_n\; \leq \;k \leq \;u_n,\; n\; \geq\; 1}$ be an array of rowwise independent, but not necessarily identically distributed, random variables with $EX_{nk}$=0 for all k and n. In this paper, we povide a domination condition under which ${\sum^{u_n}}_=u_n\; S_{nk}/n^{1/p},\; 1\; \leq\; p\;<2$ converges completely to zero.

• IMMUNE NETWORK
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• v.15 no.2
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• pp.91-99
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• 2015

Herpes simplex virus (HSV) is a common causative agent of genital ulceration and can lead to subsequent neurological disease in some cases. Here, using a genital infection model, we tested the efficacy of vinegar-processed flos of Daphne genkwa (vp-genkwa) to modulate vaginal inflammation caused by HSV-1 infection. Our data revealed that treatment with optimal doses of vp-genkwa after, but not before, HSV-1 infection provided enhanced resistance against HSV-1 infection, as corroborated by reduced mortality and clinical signs. Consistent with these results, treatment with vp-genkwa after HSV-1 infection reduced viral replication in the vaginal tract. Furthermore, somewhat intriguingly, treatment of vp-genkwa after HSV-1 infection increased the frequency and absolute number of $CD3^-NK1.1^+NKp46^+$ natural killer (NK) cells producing interferon (IFN)-${\gamma}$ and granyzme B, which indicates that vp-genkwa treatment induces the activation of NK cells. Supportively, secreted IFN-${\gamma}$ was detected at an increased level in vaginal lavages of mice treated with vp-genkwa after HSV-1 infection. These results indicate that enhanced resistance to HSV-1 infection by treatment with vp-genkwa is associated with NK cell activation. Therefore, our data provide a valuable insight into the use of vp-genkwa to control clinical severity in HSV infection through NK cell activation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.16 no.4
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• pp.734-744
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• 2002

The purpose of this study was to evaluate the protective effect of Kamicheonggan-tang(KCGT) on pre-hepatocarcinogenesis induced by N-nitrosomorpholine. The studied using blood chemistry, lipidperoxidation, antioxidant, immunohistochemistry and morphological change. The results were obtained as follows. In the pre-hepatocarcinogenesis induced by NMP, serum AST, ALT, ALP and total bilirubin were not changed in NMP and NK treated group after 1 st week, but desreased in NK treated group after 4th week as compared with NMP treated 4th week group. The content of GSH was similary to in NK treated groups as compares with data of normal group. The content of MDA was increased in NK treated group after 1st and 4th week, and more increased in the NMP treated group than those of their NK treated group. The immunohistochemically, stain of GST-p, positive lesions of KCGT were significantly decreased than those of NMP treated group. The histopathologically, fat changes, nucleotic changes, oval cell and inflammatory cells in periportal were observed in NMP treated fater 4th week, but those were significantly decreased from 4th week in the NK treated group. And the enlarged nucleus was not changed in KCGT treated group, but increased in NMP treated group after 1st and 4th week. The ultrastructurally, nucleotic changes, glycogen degeneration, lipid droplet and rER fragmentation were observed in NMP treated group after 4th week, but those changes were significantly decreased from 4th week in the NK treated group. These results suggested that KCGT extracts has protective effect on prehepatocarcinogenesis by NMP, might be usefully applied for clinical treatment of hapatic disease and also it was necessary to do more studies about its mechanisms.