• Bulletin of the Korean Mathematical Society
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• v.36 no.1
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• pp.139-146
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• 1999

It is known that a right nilpotent congruence $\beta$ on a finite algebra A is also left nilpotent [3]. The question on whether the left nilpotency class of $\beta$ in less than or equal to the right nilpotency class of $\beta$is still open. In this paper we find an upper limit for the left nilpotency class of $\beta$. In addition, under the assumption that 1 $\in$ typ{A}, we show that $(\beta]^k=[\beta)^k$ for all k$\geq$1. Thus the left and right nilpotency classes of $\beta$ are the same in this case.

• Bulletin of the Korean Chemical Society
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• v.25 no.2
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• pp.216-220
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• 2004

${\beta}$-CD and CM- ${\beta}$-CD as chiral NMR shift agents were used to resolve the enantiomers of noradrenaline (NA). The stoichiometry of each complex formed between the CDs and the enantiomers of NA was found to be 1 : 1 through the continuous variation plots. The binding constants (K) of the complexes were determined from $^1H$ NMR titration curves. This result indicated that both ${\beta}$-CD and CM- ${\beta}$-CD formed the complexes with the S(+)-NA more preferentially than its R(-)-enantiomer. The K values for the complexes with ${\beta}$-CD ($K_{S(+)}$ = 537 $M^{-1}$ and $K_{R(-)}$ = 516 $M^{-1}$ was larger than those with CM- ${\beta}$-CD ($K_{S(+)}$ = 435 $M^{-1}$ and $K_{R(-)}$ = 313 $M^{-1}$), however, enantioselectivity (${\alpha}$) of S(+)- and R(-)-NA to CM- ${\beta}$-CD ( ${\alpha}$ = 1.38) was larger than that to ${\beta}$-CD ( ${\alpha}$ = 1.04), indicating that CM- ${\beta}$-CD was the better chiral NMR solvating agents for the recognition of the enantiomers of NA. Two dimensional rotating frame nuclear Overhauser enhancement spectroscopy (ROESY) experiments were also performed to explain the binding properties in terms of spatial fitting of the NA molecule into the macrocyclic cavities.

• Korean Journal of Microbiology
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• v.27 no.1
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• pp.35-42
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• 1989

The mode of transglycosylation reaction observed during the action of low-molecular-weigh $\beta$-D-glucosidase ($\beta$-D-glucoside glucohydrolase, EC3.2.1.21) purified from Trichoderma koningii ATCC 26113 was investigated using $^{1}H$-NMR spectroscopy. The enzyme was purified by the series of procedures including ammonium sulfate precipitation, and fractionations by column chromatographies on Bio-Gel P-150, DEAE-Sephadex A-50, and SP-Sephadex C-50. The final purification was performed by the band eluation after preparative polyacrylamide gel electrophoresis. The enzyme showed its molecular size of 78,000 through the analysis of sodium dodecyl sulfate-polyacrylamide gel electrophoresis and its isoelectric point of 5.80 through the analysis of analytical isoelectric focusing. The H-1 proton resonances were analyzed. After the reaction of the enzyme with cellobiose, the reaction products were separated by high performance liquid chromatography using refractive index detector. H-1 resonances of the products were consisted with those of gentiobiose [$\beta$-D-glucopyranosyl--(1,6)-D-glucopyranose], and cellotriose [$\beta$-D glucopyranosyl-(1,4)-$\beta$-D-glucopyranosyl]-(1,4)-D-glucopyranose] with minor resonances of sophorose [$\beta$-D-glucopyranosyl-(1,2)-D-glucopyranose], respectively.

• Tuberculosis and Respiratory Diseases
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• v.45 no.4
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• pp.861-869
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• 1998

Backgrounds: The injury of a tissue results in the infalmmation, and the imflammed tissue is replaced by the normal parenchymal cells during the process of repair. But, constitutional or repetitive damage of a tissue causes the deposition of collagen resulting in the loss of its function. These lesions are found in the lung of patients with idiopathic pulmonary fibrosis, complicated fibrosis after diffuse alveolar damage (DAD) and inorganic dust-induced lung fibrosis. The tissue from lungs of patients undergoing episodes of active and/or end-stage pulmonary fibrosis shows the accumulation of inflammatory cells, such as mononuclear cells, neutrophils, mast cells and eosinophils, and fibroblast hyperplasia. In this regard, it appears that the inflammation triggers fibroblast activation and proliferation with enhanced matrix synthesis, stimulated by inflammatory mediators such as interleukin-1 (IL-1) and/or tumor necrosis factor (TNF). It has been well known that TGF-$\beta$ enhance the proliferation of fibroblasts and the production of collagen and fibronectin, and inhibit the degradation of collagen. In this regard, It is likely that TGF-$\beta$ undergoes important roles in the pathogenesis of pulmonary fibrosis. Nevertheless, this single cytokine is not the sole regulator of the pulmonary fibrotic response. It is likely that the balance of many cytokines including TGF-$\beta$, IL-1, IL-6 and TNF-$\alpha$ regulates the pathogenesis of pulmonary fibrosis. In this study, we investigate the interaction of TGF-$\beta$, IL-1$\beta$, IL-6 and TNF-$\alpha$ and their effect on the proliferation of fibroblasts. Methods: We used a human fibroblast cell line, MRC-5 (ATCC). The culture of MRC-5 was confirmed by immunofluorecent staining. First, we determined the concentration of serum in cuture medium, in which the proliferation of MRC-5 is supressed but the survival of MRC-5 is retained. Second, we measured optical density after staining the cytokine-stimulated cells with 0.5% naphthol blue black in order to detect the effect of cytokines on the proliferation of MRC-5. Result: In the medium containing 0.5% fetal calf serum, the proliferation of MRC-5 increased by 50%, and it was maintained for 6 days. IL-1$\beta$, TNF-$\alpha$ and IL-6 induced the proliferation of MRC-5 by 45%, 160% and 120%, respectively. IL-1$\beta$ and TNF-$\alpha$ enhanced TGF-$\beta$-induced proliferation of MRC-5 by 64% and 159%, but IL-6 did not affect the TGF-$\beta$-induced proliferation. And lNF-$\alpha$-induced proliferation of MRC-5 was reduced by IL-1$\beta$ in 50%. TGF-$\beta$, TNF-$\alpha$ and both induced the proliferation of MRC-5 to 89%, 135% and 222%, respectively. Conclusions: TNF-$\alpha$, TGF-$\beta$ and IL-1$\beta$, in the order of the effectiveness, showed the induction of MRC-5 proliferation of MRC-5. TNF-$\alpha$ and IL-1$\beta$ enhance the TGF-$\beta$-induced proliferation of MRC-5, but IL-6 did not have any effect TNF-$\alpha$-induced proliferation of MRC-5 is diminished by IL-1, and TNF-$\alpha$ and TGF-$\beta$ showed a additive effect.

• Applied Chemistry for Engineering
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• v.20 no.2
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• pp.195-200
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• 2009

To develop a crosslinker for the polyester powder coatings, $N^1,N^1,N^4,N^4$-tetrakis(hydroxyethyl)cyclohexane-1,4-dicarboxamide (Cy-${\beta}-HAA$), incorporated with a cyclohexane ring within the main chain of commercial ${\beta}-hydroxyalkylamide$ (${\beta}-HAA$), was prepared from the amidation of dimethyl trans-1,4-cyclohexanedicarboxylate and diethanolamine in the presence of $NaOCH_3$, The structure of $Cy-{\beta}-HAA$ was confirmed by its NMR, FT-IR and ESI-MS spectra. $Cy-{\beta}-HAA$ was thermally more stable than ${\beta}-HAA$. When $Cy-{\beta}-HAA$ was used as a crosslinker for the polyester powder coatings, it provided the smooth coating surface and reduced the formation of pinholes in the coating surface with comparison with ${\beta}-HAA$.

• Journal of Life Science
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• v.22 no.11
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• pp.1500-1506
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• 2012

Transforming growth factor (TGF)-${\beta}$-dependent apoptosis is important in the elimination of damaged or abnormal cells from normal tissues, especially in liver, in vivo. To investigate which gene expressions are critical for TGF-${\beta}$-induced apoptosis in hepatocytes, gene expression profiling experiments were performed with TGF-${\beta}$-treated and non-treated mouse hepatocytes AML12 cells. Findings showed that serum and glucocorticoid-inducible protein kinase1 (SGK1) expression is markedly downregulated during TGF-${\beta}$-induced apoptosis. Findings confirmed that expression of SGK1 protein, as well as mRNA, is also markedly decreased with TGF-${\beta}$ treatment. Infection of adenoviral vector encoding constitutively active SGK1 (CA-SGK1), but not kinase dead SGK1 (KD-SGK1), attenuated TGF-${\beta}$-induced apoptosis. All of these results suggest that downregulation of SGK1 expression is critical for TGF-${\beta}$-induced apoptosis in AML12 cells.

• BMB Reports
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• v.30 no.3
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• pp.194-199
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• 1997

Previous studies have shown that the HD3 human enterocytic differentiated colon carcinoma cell lines having low $PKC{\beta}$ activity did not respond to diacylglycerol and basic FGF by growth and by activation of pp57 MAP kinase, but undifferentiated cell lines exhibiting high $PKC{\beta}$ activity did. To confirm a role of $PKC{\beta}$ in colonocyte mitogenesis, derivatives of HD3 cell line that stably overexpress a full-length of cDNA encoding the ${\beta}_1$ isoform of human PKC were generated. The abundance and activity of $PKC{\beta}$ in two of the these cell lines, PKC3 and PKC8 were much higher than those in the C1 control cell line that carries the vector lacking the $PKC{\beta}_1\;cDNA$ insert. Following exposure to diacylglycerol or basic FGF, proliferation of PKC3 and PKC8 cells increased about 50%; but this effect was not seen with the control C1 cells. Also, in contrast to the control cells, the $PKC{\beta}_1-overproducing$ cells displayed activation of pp57 MAP kinase when treated with diacylglycerol and basic FGF as undifferentiated cell lines did. These results provide direct evidence that $PKC{\beta}_1$ which plays a key role in mitogenic responses of colon carcinoma cells to diacylglycerol and basic FGF is down-regulated in enterocytic differentiation of colon cells.

• Journal of Chest Surgery
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• v.39 no.11 s.268
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• pp.805-809
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• 2006

Background: In our previous study, we demonstrated that transforming growth factor-beta 1 receptor II(TGF-${\beta}1RII$) may have a role in the formation of bullae. In this study, we investigated if expression of transforming growth factor-beta 1 (TGF-${\beta}1$) ligand was altered in a bullous lung tissue by immunohistochemical staining of bullous tissues from patients with primary spontaneous pneumothorax. Material and Method: Bullous lung tissues were obtained from 36 patients with primary spontaneous pneumothorax, including 34 males and 2 females aged 14 to 38 years old. Result: Of the 36 patients, 19 were TGF-${\beta}1$ positive and 24 were transforming growth factor-beta 1 receptor II(TGF-${\beta}1RII$) positive. Among the 19 TGF-${\beta}1$ positives, 15 were also TGF-${\beta}1RII$ positive, observation at high magnification showed that strong immunohistochemical stain was detected in the boundary region between the bullous and normal lung tissues. Conclusion: These results suggest that overexpression of TGF-${\beta}1$ may be involved in the formation of a bulla as well as the alteration of TGF-${\beta}1RII$ expression. Further molecular studies are needed to elucidate the more detailed molecular mechanisms of the bulla formation.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.9
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• pp.4045-4048
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• 2014

Effects of transforming growth factor-beta (TGF-${\beta}$) were investigated in human colorectal cancer, and the influence of cantharidinate in inhibiting TGF-${\beta}1$ expression was explored. Relationships among TGF-${\beta}1$ and sex, age, tumor size, tumor location, tumor stage were also analyzed. H&E and immunohistochemistry staining were employed to assess colorectal cancer and TGF-${\beta}1$ expression, respectively. Then, HCT-116 CRC cells were randomly divided into four groups, controls, no serum-treated, chemotherapy and cantharidinate-treated. Immunohistochemistry and real-time PCR were employed to assess the expression of TGF-${\beta}1$ in CRC cells. Our data showed that the expression of TGF-${\beta}1$ might be associated with tumor size and tumor location (P<0.05). The expression of TGF-${\beta}1$ in CRC groups was higher than in adjacent groups (P<0.05). In addition, the expression of TGF-${\beta}1$ in cantharidinate-treated group was much lower than in CRC group (P<0.05). Taken together, these results suggest that TGF-${\beta}1$ plays an important role in CRC development. Cantharidinate might inhibit the expression of TGF-${\beta}1$ and control the development of colorectal cancer.

• Journal of Microbiology and Biotechnology
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• v.29 no.4
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• pp.562-570
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• 2019

${\beta}$-Glucosylglycerol (${\beta}-GG$) and their derivatives have potential applications in food, cosmetics and the healthcare industry, including antitumor medications. In this study, ${\beta}-GG$ and its unnatural glycosides were synthesized through the transglycosylation of two enzymes, Sulfolobus shibatae ${\beta}$-glycosidase (SSG) and Deinococcus geothermalis amylosucrase (DGAS). SSG catalyzed a transglycosylation reaction with glycerol as an acceptor and cellobiose as a donor to produce 56% of ${\beta}-GGs$ [${\beta}$-$\text\tiny{D}$-glucopyranosyl-($1{\rightarrow}1/3$)-$\text\tiny{D}$-glycerol and ${\beta}$-$\text\tiny{D}$-glucopyranosyl-($1{\rightarrow}2$)-$\text\tiny{D}$-glycerol]. In the second transglycosylation reaction, ${\beta}$-$\text\tiny{D}$-glucopyranosyl-($1{\rightarrow}1/3$)-$\text\tiny{D}$-glycerol was used as acceptor molecules of the DGAS reaction. As a result, 61% of ${\alpha}$-$\text\tiny{D}$-glucopyranosyl-($1{\rightarrow}4$)-${\beta}$-$\text\tiny{D}$-glucopyranosyl-($1{\rightarrow}1/3$)-$\text\tiny{D}$-glycerol and 28% of ${\alpha}$-$\text\tiny{D}$-maltopyranosyl-($1{\rightarrow}4$)-${\beta}$-$\text\tiny{D}$-glucopyranosyl-($1{\rightarrow}1/3$)-$\text\tiny{D}$-glycerol were synthesized as unnatural glucosylglycerols. In conclusion, the combined enzymatic synthesis of the unnatural glycosides of ${\beta}-GG$ was established. The synthesis of these unnatural glycosides may provide an opportunity to discover new applications in the biotechnological industry.