• 대한수학회논문집
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• 제33권3호
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• pp.787-798
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• 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.

• 대한수학회보
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• 제52권1호
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• pp.105-123
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• 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 $n{\in}\mathbb{N}$.

• 한국수산과학회지
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• 제34권4호
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• pp.412-418
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• 2001

[ $\beta$ ]-glucan을 시판의 배합사료에 $0.1\%$ 첨가한 다음 담수어인 잉어 (평균체중 1.0g 및 68.7g)와 해산어인 넙치 (평균 체중, 12.1 g 및 54.0g)에 2주간 첨가사료, 1주간 무첨가사료, 2주간 첨가사료 투여의 투여방법으로 5주간 경구투여한 다음 인위감염에 대한 생잔율을 조사하였다. 또 투여기간중의 말초혈액의 백혈구수와 혈중리소자임의 활성과 5주간 투여후에 채취한 백혈구의 식작용능을 조사하였다. $\beta$-glucan첨가사료 투여군에 $1\times10^6$cells의 Aeromonas hydrophila를 접종한 평균체중 68.7g의 잉어군과 $1\times10^5$cells의 Edwardsiella tarda를 접종한 평균체중 68.7g의 넙치군에서 $\beta$-glucan첨가사료 투여군이 무첨가투여군에 비해 생존율이 높았고 (P<0.05),그 외의 접종군에서는 무첨가투여군과 차이가 없었다. $\beta$-glucan첨가사료 투여기간 동안 말초혈액중의 마크로파아지와 호중구수는 투여기간에는 증가, 무투여기간에는 감소하는 경향이었으며 특히 마크로파아지의 증가가 현저하였다. 혈중 리소자임은 잉어에서는 $\beta$-glucan첨가사료 투여기간에는 상승하고 무투여기간에는 감소하였지만, $\beta$-glucan첨가사료를 다시 투여한 후 급격히 상승하여 높은 활성을 유지하였다 그러나 넙치는 잉어보다는 활성의 증가는 현저하지 않았고 무투여기간에도 변동이 없었지만 무첨가투여군보다는 항상 높은 활성을 나타내었다.

• 한국미생물·생명공학회지
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• 제28권6호
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• pp.355-360
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• 2000

Candida rugosa IFO0750의 UV-변이주를 제조하여 butyric acid를 D-$\beta$-hydroxybutyrin acid(이하 D-$\beta$-HBA)로 전환하는 데 이용하였다. 후보 변이주 중 활성이 가장 높은 Candida rugosa CM42를 이용하여 발효를 수행한 후 NMR 분석, polarimeter 분석 등을 통하여 생성된 물질이 D-$\beta$-HBA 임을 확인하였다. Chemostar 배양을 이용하여 D-$\beta$-HBA 발효 생산의 주요 영향인자를 분석하였으며, 균체의 활성을 나타내는 비생산성의 최대치는 균체의 비증식 속도를 0.06, 발효조 내의 glucose와 butyric acid의 농도를 각각 10g/L와 8.7 g/L로 각각 유지 할 때 얻어졌다. 회분식 배양 중에 glucose와 butyric acid를 공급하여 발효조 내의 glucose 및 butyric acid 농도를 최적조건으로 유지하는 fed-batch 발효를 수행하였다. 배양 180 시간 후에 D-$\beta$-HBA 농도가 약 12.4 g/L에 도달하였으며 회분식 발효에 비하여 4.7배 증가하였다.

• Journal of Applied Biological Chemistry
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• 제61권1호
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• pp.101-108
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• 2018

본 연구에서는 국내산 상황버섯의 효소 가수분해 전처리를 통한 ${\beta}-glucan$의 최적 추출조건을 확립하고 그에 따른 활성을 알아보고자 추출 조건에 따른 생이화학적활성을 측정하였다. 효소가수분해 조건을 최적화하기 위해 실시한 반응표면분석법의 결과 0.66%(v/v)의 viscozyme 농도에서 6.08시간 반응하는 것이 최적이라 예측되었으며($R^2=0.9245$), 이에 따라 최적 추출 조건에서 추출한 시료의 ${\beta}-glucan$ 함량은 1.9594 g/100 g으로 측정되었다. 추출 수율(0.76-16.40%)은 EBE가 NEBE에 비해 약 3배 높았다. ${\beta}-glucan$ 순도(11.15-59.05%)로 가장 높았으며, ${\beta}-glucan$ 함량 또한 0.26-3.38 g/100 g으로 EB (3.38 g/100 g)가 가장 높았다. 총당 함량(0.61-1.17 mg/mL)은 NEB, EB가 NEBE, EBE보다 높았으며, EB가 가장 높았다. 구성당 분석 결과, 모든 추출물에서 glucose의 함량이 가장 높았으며, 대조구와 효소 전처리구 모두 정제하면서 그 비율이 증가하였다. 단백질 함량(0.44-11.73 mg/mL)은 NEBE, EBE가 NEB, EB보다 높았으며, EBE가 가장 높았다. FT-IR 분석 결과 $890cm^{-1}$ 부근에서 peak가 확인되었기에 ${\beta}-glycosidic$ linkage를 가지고 있는 것으로 판단하였다. MTT assay를 통해 B6F10과 SK-MEL-5 세포 독성을 측정한 결과 B6F10의 경우 대조구의 세포 생존율을 100%로 하였을 때 세포 생존율이 80% 이상으로 나타나 세포독성을 보이지 않았으나, SK-MEL-5에서는 EBE를 $100{\mu}g/mL$의 농도로 처리하였을 때 세포 생존율이 75%로 나타나 약간의 세포독성을 보였다. Wound healing assay를 통해 암세포 증식 억제활성 측정 결과, 정제한 NEB, EB가 NEBE, EBE보다 활성이 높았으며, 특히 12시간일 때 EB $30{\mu}g/mL$를 처리한 경우 B6F10과 SK-MEL-5 모두에서 가장 높은 활성을 나타내었다.

• 한국식품과학회지
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• 제27권3호
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• pp.414-419
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• 1995

${\beta}-carotene$을 동결건조 당근분말로부터 초임계이산화탄소와 보조용매로서 에탄올, 메탄올을 사용하여 $40{\sim}60^{\circ}C$와 $138{\sim}276\;bar$에서 추출하였다. 초임계이산화탄소에 대한 ${\alpha},{\beta}-carotene$의 용해도는 동일온도에서 압력이 높을수록, 동일압력에서 온도가 낮을수록 증가하였다. 최고용해도는 $40^{\circ}C/276\;bar$에서 ${\alpha}-carotene$은 $0.604\;{\mu}g/g,\;{\beta}-carotene$은 $4.9\;{\mu}g/g$이었다. 보조용매로서 $CO_2$에 17.4%의 에탄올을 첨가함으로써 ${\beta}-carotene$의 용해도를 82% 이상 증가시킬 수 있었다. 위 결과는 초임계이산화탄소를 이용하여 천연물로부터 식품이나 의약산업에 중요한 특정한 카로테노이드를 추출할 수 있는 가능성을 보여주고 있다. 이와 같이 얻은 천연색소는 추출물에 잔존하는 유기용매가 없기 때문에 직접 식품가공에 이용할 수 있다.

• The Korean Journal of Physiology and Pharmacology
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• 제22권6호
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• pp.689-696
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• 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
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• 제38권2호
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• pp.105-111
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• 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
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• 제25권1호
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• pp.12-25
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• 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
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• 제26권4호
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• pp.345-354
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• 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.