• Communications of the Korean Mathematical Society
• /
• v.33 no.3
• /
• pp.787-798
• /
• 2018

For $1{\leq}p{\leq}{\infty}$, let $H^p$ be the usual Hardy space on the unit circle. When ${\alpha}$ and ${\beta}$ are bounded functions, a singular integral operator $S_{{\alpha},{\beta}}$ is defined as the following: $S_{{\alpha},{\beta}}(f+{\bar{g}})={\alpha}f+{\beta}{\bar{g}}(f{\in}H^p,\;g{\in}zH^p)$. When p = 2, we study the hyponormality of $S_{{\alpha},{\beta}}$ when ${\alpha}$ and ${\beta}$ are some special functions.

• Bulletin of the Korean Mathematical Society
• /
• v.52 no.1
• /
• pp.105-123
• /
• 2015

Let $f_{\beta}=h_{\beta}+\bar{g}_{\beta}$ and $F_a=H_a+\bar{G}_a$ be harmonic mappings obtained by shearing of analytic mappings $h_{\beta}+g_{\beta}=1/(2isin{\beta})log\((1+ze^{i{\beta}})/(1+ze^{-i{\beta}})\)$, 0 < ${\beta}$ < ${\pi}$ and $H_a+G_a=z/(1-z)$, respectively. Kumar et al. [7] conjectured that if ${\omega}(z)=e^{i{\theta}}z^n({\theta}{\in}\mathbb{R},n{\in}\mathbb{N})$ and ${\omega}_a(z)=(a-z)/(1-az)$, $a{\in}(-1,1)$ are dilatations of $f_{\beta}$ and $F_a$, respectively, then $F_a\tilde{\ast}f_{\beta}{\in}S^0_H$ and is convex in the direction of the real axis, provided $a{\in}[(n-2)/(n+2),1)$. They claimed to have verified the result for n = 1, 2, 3 and 4 only. In the present paper, we settle the above conjecture, in the affirmative, for ${\beta}={\pi}/2$ and for all $n{\in}\mathbb{N}$.

• Korean Journal of Fisheries and Aquatic Sciences
• /
• v.34 no.4
• /
• pp.412-418
• /
• 2001

The effects of dietary $\beta$-glucan administration on non-specific immune parameters in common carp, Cyprinus carpio, (1.0 g and 68.7 g of body weight) and flounder, Paralichthys olivcaces (12.1 g and 54.0 g of body weight) were evaluated. All fishes were fed an experimental diet supplemented with $\beta$-glucan at $0.1\%$ per kg diet for 5 weeks. A week intermission with basal diet occurred between first 2 weeks and second 2 weeks of $\beta$-glucan administration, The changes in the numbers of peripheral neutrophils and macrophages were counted under light microscopy and serum lysozyme activity was also analysed at a week of interval during the experiment. Phagocytic activities of leucocytes from the swimm bladder of carp and the peritonium of flounder were measured 5 weeks after feeding. The oral adminisration of $\beta$-glucan induced significant reduction in mortality after an artificial challenge with $1\times10^6$ cells of Aeromonas hydrophila in larger carp and $1\times10^5$ cells of Edwardsiella tarda in larger flounder but did not in other groups. The numbers of peripheral macrophages and neutrophils, phagocytic acitivies of leucocytes, and the activity of serum lysozyme were greatly increased in the fish fed a $\beta$-glucan supplemented diet. These suggest that $\beta$-glucan administration by oral route can enhance leucocyte phagocytic activity, serum lysozymal activity, and survival rate against artificial infections depending on the infected fish size and challenged bacterial concentration.

• Microbiology and Biotechnology Letters
• /
• v.28 no.6
• /
• pp.355-360
• /
• 2000

A UVmutant of Candida rugosa IF00750 was made and used to convert butYlic acid to D-$\beta$-hydroxybutyric acid(D-$\beta$-HBA). Major regulating factors for D-$\beta$-HBA fennentation were investigated via chemostat analyses. The maximum specific productivity was achieved at a specific growth rate of $0.06h^{-1}$ where the glucose and butyric acid concentrations in the fermentor were 10 g/L and 8.7 g/L. respectively. A fed-batch fennentation was performed with maintenance of the optimum glucose and butyric acid concentrations. The D-$\beta$-HBA concentration after 120 h of cultivation reached 12.4 g/L, which was 4.7 times greater illan the concentration obtained by batch fermentation.

• Journal of Applied Biological Chemistry
• /
• v.61 no.1
• /
• pp.101-108
• /
• 2018

This study was conducted to establish optimized ${\beta}-glucan$ extraction method through enzymatic hydrolysis from Phellinus baumii and investigate ${\beta}-glucan$ contents and physicochemical properties. The optimal condition was obtained with the enzyme concentration of 0.66% (v/v), reaction time of 6.08 h ($R^2=0.9245$) and the ${\beta}-glucan$ contents from the Phellinus baumii extracts under the optimized condition was 1.9594 g/100 g. ${\beta}-Glucan$ yield (0.76-16.40%) of enzyme beta-glucan extract (EBE) was three fold higher than that of non-enzyme beta-glucan extract (NEBE). ${\beta}-Glucan$ purity (11.15-59.05%) of non-enzyme beta-glucan (NEB) and that of enzyme beta-glucan (EB) were higher than that of NEBE and that of EBE. ${\beta}-Glucan$ purity of EB (59.05%) and ${\beta}-glucan$ contents of EB (3.38 g/100 g) showed higher than those of others. Total sugar contents (0.61-1.17 mg/mL) showed that NEB and EB were higher than that of NEBE and EBE, EB had the highest total sugar content as 1.17 mg/mL, respectively. Protein contents (0.44-11.73 mg/mL) of NEBE and that of EBE were higher than that of NEB, that of EB. In FT-IR spectrum, the band at $890cm^{-1}$ of microcapsule was attributed to a ${\beta}-1,3-glucan$. The toxicities of ${\beta}-glucan$ from Phellinus baumii in both melanoma cell lines was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoli um bromide assay and ${\beta}-glucan$ from Phellinus baumii has no toxicity until $30{\mu}g/mL$. The effects of ${\beta}-glucan$ from Phellinus baumii on inhibition of cancer cell proliferation were detected by using a wound healing assay. The effect of NEB and EB were higher than NEBE and EBE, especially $30{\mu}g/mL$ of EB had the highest in both melanoma cell lines.

• Korean Journal of Food Science and Technology
• /
• v.27 no.3
• /
• pp.414-419
• /
• 1995

${\beta}-carotene$ was extracted from freeze-dried carrot by supercritical carbon dioxide $(SC-CO_2)$ and mixtures of $CO_2$ doped with ethanol or methanol as a cosolvent at temperatures of 40 to $60^{\circ}C$ and pressures of 138 to 276 bar. Solubility of ${\beta}-carotene$ in $SC-CO_2$ increased with the increase of extraction pressure and the decrease of extraction temperature. The highest solubility observed was $4.90\;{\mu}g/g\;CO_2\;for\;{\alpha}-carotene\;and\;0.604\;{\mu}g/g\;CO_2$ for ${\alpha}-carotene\;at\;40^{\circ}C$ and 276 bar. Addition of ethanol increased the solubility being the largest increase of 82% using a mixture of $CO_2$ and 17.4% ethanol. $SC-CO_2$ extraction can be used to selectively obtain natural carotenoids, free of solvent residuals, which can be used as food additives.

• The Korean Journal of Physiology and Pharmacology
• /
• v.22 no.6
• /
• pp.689-696
• /
• 2018

Increasing evidence implicates changes in $[Ca^{2+}]_i$ and oxidative stress as causative factors in amyloid beta ($A{\beta}$)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting $Ca^{2+}$ and $Zn^{2+}$ signaling. The present study aimed to determine whether C3G exerts a protective effect against $A{\beta}_{25-35}$-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for $Ca^{2+}$, $Zn^{2+}$, MMP and ROS. Treatment with $A{\beta}_{25-35}$ ($20{\mu}M$) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited $A{\beta}_{25-35}$-induced $[Zn^{2+}]_i$ increases as well as $[Ca^{2+}]_i$ increases in the cultured rat hippocampal neurons. C3G also significantly inhibited $A{\beta}_{25-35}$-induced mitochondrial depolarization. C3G also blocked the $A{\beta}_{25-35}$-induced formation of ROS. In addition, C3G significantly inhibited the $A{\beta}_{25-35}$-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid ${\beta}$-induced neuronal cell death by reducing multiple apoptotic signals.

• Molecules and Cells
• /
• v.38 no.2
• /
• pp.105-111
• /
• 2015

The beta2-adrenergic receptor (${\beta}2AR$) belongs to the G protein coupled receptor (GPCR) family, which is the largest family of cell surface receptors in humans. Extra attention has been focused on the human GPCRs because they have been studied as important protein targets for pharmaceutical drug development. In fact, approximately 40% of marketed drugs directly work on GPCRs. GPCRs respond to various extracellular stimuli, such as sensory signals, neurotransmitters, chemokines, and hormones, to induce structural changes at the cytoplasmic surface, activating downstream signaling pathways, primarily through interactions with heterotrimeric G proteins or through G-protein independent pathways, such as arrestin. Most GPCRs, except for rhodhopsin, which contains covalently linked 11 cis-retinal, bind to diffusible ligands, having various conformational states between inactive and active structures. The first human GPCR structure was determined using an inverse agonist bound ${\beta}2AR$ in 2007 and since then, more than 20 distinct GPCR structures have been solved. However, most GPCR structures were solved as inactive forms, and an agonist bound fully active structure is still hard to obtain. In a structural point of view, ${\beta}2AR$ is relatively well studied since its fully active structure as a complex with G protein as well as several inactive structures are available. The structural comparison of inactive and active states gives an important clue in understanding the activation mechanism of ${\beta}2AR$. In this review, structural features of inactive and active states of ${\beta}2AR$, the interaction of ${\beta}2AR$ with heterotrimeric G protein, and the comparison with ${\beta}1AR$ will be discussed.

• Biomolecules & Therapeutics
• /
• v.25 no.1
• /
• pp.12-25
• /
• 2017

G protein-coupled receptors (GPCRs) are a family of cell-surface proteins that play critical roles in regulating a variety of pathophysiological processes and thus are targeted by almost a third of currently available therapeutics. It was originally thought that GPCRs convert extracellular stimuli into intracellular signals through activating G proteins, whereas ${\beta}$-arrestins have important roles in internalization and desensitization of the receptor. Over the past decade, several novel functional aspects of ${\beta}$-arrestins in regulating GPCR signaling have been discovered. These previously unanticipated roles of ${\beta}$-arrestins to act as signal transducers and mediators of G protein-independent signaling have led to the concept of biased agonism. Biased GPCR ligands are able to engage with their target receptors in a manner that preferentially activates only G protein- or ${\beta}$-arrestin-mediated downstream signaling. This offers the potential for next generation drugs with high selectivity to therapeutically relevant GPCR signaling pathways. In this review, we provide a summary of the recent studies highlighting G protein- or ${\beta}$-arrestin-biased GPCR signaling and the effects of biased ligands on disease pathogenesis and regulation.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
• /
• v.26 no.4
• /
• pp.345-354
• /
• 2000

TGF-${\beta}_1$ is a potent chemotactic factor for inflammatory cells and fibroblasts. It also stimulates the celluar source and components of extracellular matrix and the production of proteinase inhibitors. Collectively, these biologic activities lead to the accumulation and stabilization of the nascent matrix, which is vital to wound healing. The objective of this study is to investigate production of TGF-${\beta}_1$ in vitro fibroblast culture in the presence of Staphylococcus enterotoxin B(SEB) and/or lipopolysaccharide(LPS) and to elucidate the role of TGF-${\beta}_1$ which may be responsible for wound healing. The fibroblasts were originated from facial dermis and hypertrophic scar in 26 year-old male patient. In the presence of LPS($0.01{\mu}g$, $0.1{\mu}g$, $1.0{\mu}g$), SEB($0.01{\mu}g$, $0.1{\mu}g$, $1.0{\mu}g$) respectively, cells($5{\times}10^3ml$) were cultivated in vitro. At 1, 3, and 5 days after incubation, cells were counted. Also, cells($2.5{\times}10^5ml$) were cultivated in EMEM with LPS(0.01, 0.1 and $1.0{\mu}g$), SEB(0.01, 0.1 and $1.0{\mu}g$) respectively and LPS($0.1{\mu}g$) and SEB($0.1{\mu}g$) in combination for 24, 48, and 72 hours respectively. Culture supernatants were harvested at 1, 2, and 3 days after incubation period and triplicate culture supernatants were pooled and TGF-${\beta}_1$ was assayed in duplicate. The results were as follows. 1. In facial dermal fibroblast induced with SEB and LPS respectively or in combination, the suppression of cell proliferation occurred very significantly at 1 day after incubation, compared with the control. In SEB exposure, the production of TGF-${\beta}_1$ was decreased very significantly at 1 day after incubation, compared with the control. However, in LPS, SEB and LPS exposure, the production of TGF-${\beta}_1$ was increased very significantly at 1 day after incubation, compared with the control. 2. In hypertrophic scar fibroblast induced with SEB and LPS respectively or in combination, the suppression of cell proliferation did not occur at 1 day after incubation, compared with the control. In SEB and LPS exposure in combination, the production of TGF-${\beta}_1$ was increased very significantly at 1 day after incubation, compared with the control. However, the production of TGF-${\beta}_1$ did not occur in SEB and LPS exposure respectively. In conclusion, the concentration of bacterial toxins and the incubation period correlated with cell proliferation and production of TGF-${\beta}_1$ very significantly and both fibroblasts have different phenotype each other in this regard. This data suggest that the significant production of TGF-${\beta}_1$ may develope abnormal wound healing associated with tissue fibroproliferative disorder, such as hypertrophic scar and keloid formation.