• IMMUNE NETWORK
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• v.6 no.1
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• pp.1-5
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• 2006

Background: B cell subset has been divided into B-1 cells and B-2 cells. B-1 cells are found most prominently in the peritoneal cavity, as well as constituting a small pro portion of splenic B cells and they are larger and less dense than B-2 cells in morphology. This study was designed to compare the differences in their proliferation and differentiation between B-1 and B-2 cell. Methods: We obtained sorted B-1 cells from peritoneal fluid and B-2 cells from spleens of mice. Secreted IgM was measured by enzyme-linked immunosorbent assay. Entering of S phase in response to LPS-stimuli was measured by proliferative assay. Cell cycle analysis by propidium iodide was performed. p21 expression was assessed by real time PCR. Results: Cell proliferation and cell cycle progression in B-1 and B-2 cells, which did not occur in the absence of LPS, required LPS stimulation. After LPS stimulation, B-1 and B-2 cells were shifted to Sand G2/M phases. p21 expression by resting B-1 cells was higher than that of resting B-2 cells. Conclusion: B-1 cells differ from conventional B-2 cells in proliferation, differentiation and cell cycle.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.1
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• pp.157-166
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• 2004

In order to understand the anti-carcinogenic effects of Boo-jung-bae-bon-bang(扶正培本方)-B1), Hwal-hyul-hwa-eo-bang(活血化瘀方-B2), Cheong-youl-hae-dok-bang(淸熱解毒方-B3), prescriptions of individual B1, B2, and B3 treatments or combined treatments (B4; B1+B2, B5; B1+B3, B6; B1+B2+83, B7; B2+83) were applied to cultured cancer cell lines. The major findings on their anti-cardnogenic effects in terms of mechanism and synergistic interactions are summarized below. Results of cytokine gene expression analyses are summarized as follows; IL-2 gene expression was increased by B1 and B6 treatments, IFN-v gene expression increased by B3, B1, B6, and 85, and CD28 gene expression increased by B1 and B5. IL-4 expression was not affected by any treatments. In the FACS analysis, increases in numbers of immunoreactive CD3/sup +//CD25/sup +/ T cells by B1 and B5 treatment, CD3/sup +//CD69/sup +/ T cells by B1, B3, B5, and B6 treatments, CD19/sup +//CD44/sup +/ B cells by B1 and B6 treatments were observed when compared to the corresponding non-treated control groups.

• Bulletin of the Korean Chemical Society
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• v.8 no.3
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• pp.185-189
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• 1987

Reactions of $Ir(ClO)_4(CO)(PPh_3)_2$ with dicyano olefins, cis-NCCH = CH$CH_2$$CH_2$CN (cDC1B), trans-NCCH = CH$CH_2$$CH_2$CN (tDC1B), trans-NC$CH_2$CH = CH$CH_2$CN (tDC2B), and NC$CH_2$$CH_2$$CH_2$$CH_2$CN (DCB) produce binuclear dicationic iridium (I) complexes, $[(CO)(PPh_3)_2Ir-NC-A-CN-Ir(PPh_3)_2(CO)](ClO_4)_2$ (NC-A-CN = cDC1B (1a), tDC1B (1b), tDC2B (1c), DCB (1d)). Complexes 1a-1d react with hydrogen to give binuclear dicationic tetrahydrido iridium (Ⅲ ) complexes, $[(CO)(PPh_3)_2(H)_2Ir-NC-A-CN-Ir(H)_2(PPh_3)_2(CO)](ClO_4)_2$ (NC-A-CN = cDC1B (2a), tDC1B (2b), tDC2B (2c), DCB (2d)). Complexes 2a and 2b catalyze the hydrogenation of cDC1B and tDC1B, respectively to give DCB, while the complex 2c is catalytically active for the isomerization of tDC2B to give cDC1B and tDC1B and the hydrogenation of tDC2B to give DCB at $100^{\circ}C$.

• Kyungpook Mathematical Journal
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• v.54 no.4
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• pp.521-529
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• 2014

In this paper we derive some optimal convex combination bounds related to arithmetic mean. We find the greatest values ${\alpha}_1$ and ${\alpha}_2$ and the least values ${\beta}_1$ and ${\beta}_2$ such that the double inequalities $${\alpha}_1T(a,b)+(1-{\alpha}_1)H(a,b)<A(a,b)<{\beta}_1T(a,b)+(1-{\beta}_1)H(a,b)$$ and $${\alpha}_2T(a,b)+(1-{\alpha}_2)G(a,b)<A(a,b)<{\beta}_2T(a,b)+(1-{\beta}_2)G(a,b)$$ holds for all a,b > 0 with $a{\neq}b$. Here T(a,b), H(a,b), A(a,b) and G(a,b) denote the second Seiffert, harmonic, arithmetic and geometric means of two positive numbers a and b, respectively.

• IMMUNE NETWORK
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• v.4 no.3
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• pp.155-160
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• 2004

Background: B-1 cells differ from conventional B-2 cells both phenotypically and functionally. The aim of this study was to investigate the difference between peritoneal B-1 cells and splenic B-2 cells in proliferation. Methods: We obtained sorted B-1 cells from peritoneal fluid and B-2 cells from spleens of mice. During the culture of these cells, immunoglobulin secreted into the culture supernatants was evaluated by enzymelinked immunosorbent assay. Entering of S phase in response to LPS-stimuli was measured by proliferative assay. Results: Spontaneous Immunoglobulin M production occurred in peritoneal B-1 cells but not in splenic B-2 cells. LPS stimulated peritoneal B-1 cells secreted IgM at day 1, but splenic B-2 cells at day 2. In thymidine incorporation, peritoneal B-1 cells entered actively S phase after 24hours LPS-stimulation but splenic B-2 cells entered actively S phase after 48 hours. Conclusion: IgM secretion and S phase entering occurred early in peritoneal B-1 cells compared to splenic B-2 cells.

• Toxicological Research
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• v.12 no.1
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• pp.17-20
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• 1996

The effect of Fumonisin B1, a mycotoxin produced by Fusarium moniliforme on bacterial viruses P1 and Lambda, was investigated by the virus plaque assay. Fumonisin B1 inhibited the P1 viral multiplication in the concentration range from $100{\mu}g$/ml to $400{\mu}g$/ml. The inhibition was Fumonisin B1 concentration-dependent. Another bacterial virus Lambda multiplication was also inhibited by lower concentration of Fumonisin B1 ($10{\mu}g$/ml~$50{\mu}g$/ml). This inhibition was dependent on Fumonisin B1 and on virus-Fumonisin B1 reaction time. Sensitivity of bacteriophage Lambda to Fumonisin B1 was higher than that of P1 virus. Lambda vital DNA was treated in vitro with Fumonisin B1 at various concentration. Significant DNA fragmentation by Fumonisin 191 was observed in the agarose gel electrophoresis. Lambda viral DNA was partially digested even in the Fumonisin B1 $10{\mu}g$ and the level of its fragmentation was dependent on Fumonisin B1 amount up to $30{\mu}g$ per assay.

• The Journal of the Institute of Internet, Broadcasting and Communication
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• v.11 no.4
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• pp.157-164
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• 2011

It is very difficult problem to factorize composite number. Integer factorization algorithms, for the most part, find ($a,b$) that is congruence of squares ($a^2{\equiv}b^2$(mode $n$)) with using factoring(factor base, B) and get the result, $p=GCD(a-b,n)$, $q=GCD(a+b,n)$ with taking the greatest common divisor of Euclid based on the formula $a^2-b^2=(a-b)(a+b)$. The efficiency of these algorithms hangs on finding ($a,b$). Fermat's algorithm that is base of congruence of squares finds $a^2-b^2=n$. This paper proposes the method to find $a^2-b^2=kn$, ($k=1,2,{\cdots}$). It is supposed $b_1$=0 or 5 to be surely, and b is a double number. First, the proposed method decides $k$ by getting kn that satisfies $b_1=0$ and $b_1=5$ about $n_2n_1$. Second, it decides $a_2a_1$ that satisfies $a^2-b^2=kn$. Third, it figures out ($a,b$) from $a^2-b^2=kn$ about $a_2a_1$ as deciding $\sqrt{kn}$ < $a$ < $\sqrt{(k+1)n}$ that is in $kn$ < $a^2$ < $(k+1)n$. The proposed algorithm is much more effective in comparison with the conventional Fermat algorithm.

• Journal of the Korean Mathematical Society
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• v.47 no.2
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• pp.263-275
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• 2010

Let {$X_n;n\;\geq\;1$} be a strictly stationary sequence of negatively associated random variables with mean zero and finite variance. Set $S_n\;=\;{\sum}^n_{k=1}X_k$, $M_n\;=\;max_{k{\leq}n}|S_k|$, $n\;{\geq}\;1$. Suppose $\sigma^2\;=\;EX^2_1+2{\sum}^\infty_{k=2}EX_1X_k$ (0 < $\sigma$ < $\infty$). We prove that for any b > -1/2, if $E|X|^{2+\delta}$(0<$\delta$$\leq$1), then $$lim\limits_{\varepsilon\searrow0}\varepsilon^{2b+1}\sum^{\infty}_{n=1}\frac{(loglogn)^{b-1/2}}{n^{3/2}logn}E\{M_n-\sigma\varepsilon\sqrt{2nloglogn}\}_+=\frac{2^{-1/2-b}{\sigma}E|N|^{2(b+1)}}{(b+1)(2b+1)}\sum^{\infty}_{k=0}\frac{(-1)^k}{(2k+1)^{2(b+1)}}$$ and for any b > -1/2, $$lim\limits_{\varepsilon\nearrow\infty}\varepsilon^{-2(b+1)}\sum^{\infty}_{n=1}\frac{(loglogn)^b}{n^{3/2}logn}E\{\sigma\varepsilon\sqrt{\frac{\pi^2n}{8loglogn}}-M_n\}_+=\frac{\Gamma(b+1/2)}{\sqrt{2}(b+1)}\sum^{\infty}_{k=0}\frac{(-1)^k}{(2k+1)^{2b+2'}}$$, where $\Gamma(\cdot)$ is the Gamma function and N stands for the standard normal random variable.

• Toxicological Research
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• v.33 no.3
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• pp.211-218
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• 2017

Cytochrome P450 1B1 (CYP1B1) acts as a hydroxylase for estrogen and activates potential carcinogens. Moreover, its expression in tumor tissues is much higher than that in normal tissues. Despite this association between CYP1B1 and cancer, the detailed molecular mechanism of CYP1B1 on cancer progression in HeLa cells remains unknown. Previous reports indicated that the mRNA expression level of Herc5, an E3 ligase for ISGylation, is promoted by CYP1B1 suppression using specific small interfering RNA, and that ISGylation may be involved in ubiquitination related to ${\beta}-catenin$ degradation. With this background, we investigated the relationships among CYP1B1, Herc5, and ${\beta}-catenin$. RT-PCR and western blot analyses showed that CYP1B1 overexpression induced and CYP1B1 inhibition reduced, respectively, the expression of $Wnt/{\beta}-catenin$ signaling target genes including ${\beta}-catenin$ and cyclin D1. Moreover, HeLa cells were treated with the CYP1B1 inducer $7,12-dimethylbenz[{\alpha}]anthracene$ (DMBA) or the CYP1B1 specific inhibitor, tetramethoxystilbene (TMS) and consequently DMBA increased and TMS decreased ${\beta}-catenin$ and cyclin D1 expression, respectively. To determine the correlation between CYP1B1 expression and ISGylation, the expression of ISG15, a ubiquitin-like protein, was detected following CYP1B1 regulation, which revealed that CYP1B1 may inhibit ISGylation through suppression of ISG15 expression. In addition, the mRNA and protein expression levels of Herc5 were strongly suppressed by CYP1B1. Finally, an immunoprecipitation assay revealed a direct physical interaction between Herc5 and ${\beta}-catenin$ in HeLa cells. In conclusion, these data suggest that CYP1B1 may activate $Wnt/{\beta}-catenin$ signaling through stabilization of ${\beta}-catenin$ protein from Herc5-mediated ISGylation for proteosomal degradation.

• Korean Journal of Clinical Pharmacy
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• v.24 no.4
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• pp.231-239
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• 2014

Background and objective: Pravastatin has been shown to have favorable risk-benefit profile when it is administered to hypercholesterolemic subjects to prevent cardiovascular events. However, subjects with impaired OATP1B1 activity may be more susceptible to pravastatin-induced muscle toxicity than subjects with normal OATP1B1 activity. A systematic review was conducted to evaluate the effect of SLCO1B1 genetic polymorphism on pharmacokinetics of pravastatin. Method: Medline$^{(R)}$ and Embase$^{(R)}$ were searched for relevant studies until July 2013. The search terms used were pravastatin AND (SLCO1B1 OR OATP1B1 OR LST1 OR SLC21A6) AND (gene OR $genetic^*$ OR $genomic^*$ OR $pharmacogenet^*$ OR $pharmacogenom^*$ OR $polymorph^*$). Results: A meta-analysis of the area under the concentration-time curve (AUC) of pravastatin in $SLCO1B1^*15$ and $SLCO1B1^*1a/^*1a$ was conducted. Five studies met all the inclusion criteria and methodological requirements. There was no statistically significant difference in the AUC value between $SLCO1B1^*15$ and $SLCO1B1^*1a/^*1a$ (p=0.728). However, $SLCO1B1^*15$ participants exhibited significantly higher AUC values than $SLCO1B1^*1b/^*1b$ carriers (p<0.001). In case of $SLCO1B1^*15^*15$ carriers, they had significantly higher AUC value than $SLCO1B1^*1a/^*1a$ subjects (p=0.002). Lastly, compared with to the subjects of $SLCO1B1^*1a/^*1a$, the carriers of heterozygous $SLCO1B1^*15$ increased the AUC value of pravastatin statistically significantly in Asian population (p=0.014). Conclusion: The present meta-analysis suggests that subjects with $SLCO1B1^*15$ are associated with increased AUC of pravastatin.