• Archives of Pharmacal Research
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• v.22 no.4
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• pp.423-427
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• 1999

A study was carried out to evaluate flavonol glycosides in leaves of Symplocarpus renifolius (Araceae). From the water fraction of the MeOH extract, three new flavonol glycosides were isolated along with three known compounds, Kaempferol-3-O-$\beta$-glucopyranosyl-($1{\rightarrow}2$)-$\beta$-D-glucopyranosyl-7-O-$\beta$-D-glucopyranoside, quercetin-3-O-$\beta$-D-glucopyranosy-1-($1{\rightarrow}2$)-$\beta$-D-glucopyranoside, and caffeic acid. The structures of the new flavonol glycosides were elucidated by chemical and spectral analyses a quercetin-3-O-$\beta$-D-glucopyranosyl-($1{\rightarrow}2$)-$\beta$-D-glucopyranosyl-7-O-$\beta$-D-glucopyranoside, isorhamnetin-3-O-$\beta$-D-glucopyranosyl-(1 2)-$\beta$-D-glucopyranosyl-7-O-$\beta$-D-glucopyranosdie, and quercetin-3-O$\beta$-D-glucopyranosyl-($1{\rightarrow}2$)-$\beta$-D-glycopyranosyl-7-O-($6^{IIII}$-trans-caffeoyl)-$\beta$-D-glucopyranoside.

• 월간산업보건
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• s.296
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• pp.10-13
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• 2012

N-phenyl-${\beta}$-naphthylamine(PBNA)의 수치화된 직업적 노출기준은 권고하지 않았다. 공업용 N-phenyl-${\beta}$-naphthylamine에는 불순물로 ${\beta}$-Naphthylamine포함되어 있다. ${\beta}$-Naphthylamine은 사람에서 발암성 확인물질(A1)로 ${\beta}$-Naphthylamine에 대한 TLV Documentation의 참조가 필요하다. ${\beta}$-Naphthylamine은 N-phenyl-${\beta}$-naphthylamine에 노출된 사람의 대사산물이다. N-phenyl-${\beta}$-naphthylamine은 동물실험에서 제한적으로 발암성이 증명되었지만 사람에서는 발암성이 충분하게 입증되지는 않았다. 따라서 사람에게 발암성으로 분류되지 않는 A4로 경고주석을 선정하였으며 수치화된 노출기준 없이 모든 노출경로에서 N-phenyl-${\beta}$-naphthylamine에 노출되지 않도록 관리하는 것을 권고하였다.

• Journal of Chest Surgery
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• v.43 no.4
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• pp.394-398
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• 2010

Background: The overexpression of transforming growth factor-beta 1 receptor II (TGF-${\beta}1$RII) and transforming growth factor-beta 1 (TGF-${\beta}1$) ligand may be involved in the formation of a bulla. In this study, we tested if serum TGF-${\beta}1$ ligand levels correlated with the expression level of TGF-${\beta}1$RII and TGF-${\beta}1$ in bullous tissues from patients with spontaneous pneumothorax. Material and Method: Bullous lung tissues and blood samples were obtained from 19 patients with spontaneous pneumothorax, 18 males and 1 female, aged 17 to 35 years old. The bullous tissues were obtained by video-assisted thoracic surgery (VATS), fixed in formalin, embedded in paraffin, and cut into $5{\sim}6{\mu}m$ thick slices. Sections were immunohistochemically stained with primary antibodies against TGF-${\beta}1$ or TGF-${\beta}1$RII, and serum levels of TGF-${\beta}1$ in patients and normal controls was measured by enzyme-linked immunosorbent assay (ELISA). Result: Of the 19 patients, 16 were TGF-${\beta}1$ positive and 10 were TGF-${\beta}1$RII positive. Among the 16 TGF-${\beta}1$ positives, 9 were also TGF-${\beta}1RII$ positive. As seen previously, strong immunohistochemical staining of TGF-${\beta}1$RII and TGF-${\beta}$ was detected in the boundary region between the bullous and normal lung tissues. Average TGF-${\beta}1$ blood levels of both TGF-${\beta}1$ and TGF-${\beta}1$RII positive patients was $38.36{\pm}16.2ng/mL$, and that of five controls was $54.06{\pm}15ng/mL$. Conclusion: These results suggest that overexpression of TGF-${\beta}1$ and TGF-${\beta}1$RII expression may be involved in the formation of bullae. TGF-${\beta}1$ blood levels in patients with primary spontaneous pneumothorax is lower than normal people, suggesting that the high level of local TGF-${\beta}1$ expression in the bullous tissue region, but not in the whole blood, may contribute more in the formation of bullae.

• Food Science and Biotechnology
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• v.15 no.3
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• pp.437-440
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• 2006

To explore the possible usefulness of ${\beta}$-glucans as natural antioxidants, the antioxidant profiles of ${\beta}$-glucan, extracted from Saccharomyces cerevisiae KCTC 7911, and water soluble and insoluble mutant ${\beta}$-glucan, isolated from yeast mutant S. cerevisiae IS2, were examined by five different in vitro evaluation methods: lipid peroxidation value (POV), nitric oxide (NO), 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, reducing power, and ${\beta}$-carotene diffusion assay. The antioxidant activities of all ${\beta}$-glucans evaluated in POV test were comparable to or better than that of the known antioxidant, vitamin C. Remarkably, the ${\beta}$-glucan and water insoluble mutant ${\beta}$-glucan possessed 2.5-fold more potent activity than vitamin C at a dosage of 2 mg. Although vitamin C showed 100-fold greater activity than all ${\beta}$-glucans in NO and DPPH tests for measuring the radical scavenging capacity, all ${\beta}$-glucans revealed higher radical scavenging activity than the known radical scavenger, N-acetyl-L-cysteine (NAC), in DPPH test. The water insoluble mutant ${\beta}$-glucan had 2.6- and 5-fold greater antioxidative activity than water soluble ${\beta}$-glucan in NO and DPPH tests, respectively, showing that all ${\beta}$-glucans were able to scavenge radicals such as NO or DPPH. While all ${\beta}$-glucans revealed lower antioxidant profiles than vitamin C in both reducing power activity and ${\beta}$-carotene agar diffusion assay, the ${\beta}$-glucan and water insoluble mutant ${\beta}$-glucan did show a marginal reducing power activity as well as a considerable ${\beta}$-carotene agar diffusion activity. These results confirmed the potential usefulness of these ${\beta}$-glucans as natural antioxidants.

• Journal of the Korean Chemical Society
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• v.23 no.5
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• pp.307-313
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• 1979

Seven new hydrazine derivatives were prepared from N-Aryllsufonylbenzimidoyl chloride. These were: ${\beta}-({\alpha}-Benzenesulfonamidobenzal)hydrazine\;(II),\;{\beta}-({\alpha}-Benzenesulfonamidobenzal)dimethylmethylenehydrazine\;(III),\;{\beta}-({\alpha}-Benzenesulfonamidobenzal)phenylhydrazine\;(VII),\;{\beta}-({\alpha}-Benzenesulfonamidobenzal)-4-nitrophenylhydrazine\;(VIII),\;{\beta}-({\alpha}-Benzenesulfonamidobenzal)-2,4-dinitrophenylhydrazine\;(IX),\;{\beta}-({\alpha}-Benzenesulfonamidobenzal)dimethylhydrazine\;(X),\;{\beta}-({\alpha}-Benzenesulfonamidobenzal)-p-methylphenylhydrazine\;(XI)$. The structure of these derivatives were identified by elemental analysis, spectral data and other chemical methods. In general, it was found that the yields of these reactions were significantly improved in polar solvent and by the electron attracting substituents in phenylhydrazine.

• Journal of the Korean Society of Food Science and Nutrition
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• v.26 no.2
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• pp.270-284
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• 1997

Effects of dietary carotenoids were investigated on the metaboβsm and body pigmentation of rainbow trout(Salmo gairdneri), masu salmon(Oncorhynchus macrostomos), eel(Anguilla japonica), rock fish(Sebastes inermis) and black rock fish(Sebastes schlegeli). Three weeks later after depletion, these fishes were fed diet supplemented with ${\beta}-carotene$, lutein, canthaxanthin', astaxanthin or ${\beta}-apo-8'-carotenal$ for 4 to 5 weeks, respectively. Carotenoids distributed to and changed in integument were analyzed. In the integument of rainbow trout. zeaxanthin, ${\beta}-carotene$ and canthaxanthin were found to be the major carotenoids, while lutein, isocryptoxanthin and salmoxanthin were the minor carotenoids. In the integument of masu salmon, zeaxanthin was found to be the major carotenoids, while triol, lutein, tunaxanthin, ${\beta}-carotene$, ${\beta}-cryptoxanthin$ and canthaxanthin were the minor carotenoids. In the integument of eel, ${\beta}-carotene$ was found to be the major carotenoids, while lutein, zeaxanthin and ${\beta}-cryptoxanthin$ were the minor carotenoids. In the integument of rock fish, zeaxanthin, ${\beta}-carotene$, tunaxanthin$(A{\sim}C)$ and lutein were found to be the major carotenoids, while ${\beta}-cryptoxanthin$, ${\alpha}-cryptoxanthin$ and astaxanthin were the minor carotenoids. Likely in the integument of black rock fish, ${\beta}-carotene$, astaxanthin and zeaxanthin were found to be the major carotenoids, whereas ${\alpha}-cryptoxanthin$, ${\beta}-cryptoxanthin$, lutein and canthaxanthin were the minor contributor. The efficacy of body pigmentation by the accumulation of carotenoids in the integument of rainbow trout and masu salmon were the most effectively shown in the canthaxanthin group and of eel, rock fish and black rock fish were the most effectively shown in the lutein group. Based on these results in the integument of each fish, dietary carotenoids were presumably biotransformed via oxidative and reductive pathways. In the rainbow trout, ${\beta}-carotene$ was oxidized to astaxanthin via successively isocryptoxanthin, echinenone and canthaxanthin. Lutein was oxidized to canthaxanthin. Canthaxanthin was reduced to ${\beta}-carotene$ via isozeaxanthin, and astaxanthin was reduced to zeaxanthin via triol. In the masu salmon, ${\beta}-carotene$ was oxidized to zeaxanthin. Lutein was reduced to zeaxanthin via tunaxanthin. Canthaxanthin was reduced to zeaxanthin via ${\beta}-carotene$. and astaxanthin was reduced to zeaxanthin via triol. In the eel, ${\beta}-carotene$ and lutein were directly deposited but canthaxanthin was reduced to ${\beta}-carotene$, and cholesterol lowering effect by Meju supplementation might be resulted from the modulation of fecal axanthin, astaxanthin and ${\beta}-apo-8'-carotenal$ were oxidized and reduced to tunaxanthin via zeaxanthin. In the black roch fish, ${\beta}-carotene$ was oxidized to ${\beta}-cryptoxanthin$. Lutein was reduced to ${\beta}-carotene$ via ${\alpha}-cryptoxanthin$. Canthaxanthin was reduced to ${\alpha}-cryptoxanthin$ via successively ${\beta}-cryptoxanthin$ and zeaxanthin. Astaxanthin converted to tunaxanthin via isocryptoxanthin and zeaxanthin, and ${\beta}-apo-8'-carotenal$ was reduced to ${\alpha}-cryptoxanthin$ via ${\beta}-cryptoxanthin$ and zeaxanthin.

• Bulletin of the Korean Mathematical Society
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• v.34 no.4
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• pp.627-636
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• 1997

Let $H(U)$ be the space of all analytic functions in the unit disk $U$ and let $K \subset H(U)$. For the operator $A_{\beta,\gamma} : K \longrightarrow H(U)$ defined by $$ A_{\beta,\gamma}(f)(z) = [\frac{z^\gamma}{\beta + \gamma} \int_{0}^{z} f^\beta (t)t^{\gamma-1} dt]^{1/\beta} $$ and $\beta,\gamma \in C$, we determined conditions on g(z), $\beta and \gamma$ such that $$ z[\frac{z}{f(z)]^\beta \prec z[\frac{z}{g(z)]^\beta implies z[\frac{z}{A_{\beta,\gamma}(f)(z)]^\beta \prec z[\frac{z}{A_{\beta,\gamma}(g)(z)]^\beta $$ and we presented some particular cases of our main result.

• East Asian mathematical journal
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• v.31 no.1
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• pp.103-107
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• 2015

We use some known contiguous function relations for $_2F_1$ to show how simply the following three recurrence relations for Jacobi polynomials $P_n^{({\alpha},{\beta)}(x)$: (i) $({\alpha}+{\beta}+n)P_n^{({\alpha},{\beta})}(x)=({\beta}+n)P_n^{({\alpha},{\beta}-1)}(x)+({\alpha}+n)P_n^{({\alpha}-1,{\beta})}(x);$ (ii) $2P_n^{({\alpha},{\beta})}(x)=(1+x)P_n^{({\alpha},{\beta}+1)}(x)+(1-x)P_n^{({\alpha}+1,{\beta})}(x);$ (iii) $P_{n-1}^{({\alpha},{\beta})}(x)=P_n^{({\alpha},{\beta}-1)}(x)+P_n^{({\alpha}-1,{\beta})}(x)$ can be established.

• Proceeding of EDISON Challenge
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• 2014.03a
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• pp.237-249
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• 2014

Deposition of amyloid-${\beta}$ ($A{\beta}$) proteins is the conventional pathological hallmark of Alzheimer's disease (AD). The $A{\beta}$ protein formed from the amyloid precursor protein is predominated by the 40 residue protein ($A{\beta}40$) and by the 42 residue protein ($A{\beta}42$). While $A{\beta}40$ and $A{\beta}42$ differ in only two amino acid residues at the C-terminal end, $A{\beta}42$ is much more prone to aggregate and exhibits more neurotoxicity than $A{\beta}40$. Here, we investigate the molecular origin of the difference in the aggregation propensity of these two proteins by performing fully atomistic, explicit-water molecular dynamics simulations. Then, it is followed by the solvation thermodynamic analysis based on the integral-equation theory of liquids. We find that $A{\beta}42$ displays higher tendency to adopt ${\beta}$-sheet conformations than $A{\beta}40$, which would consequently facilitate the conversion to the ${\beta}$-sheet rich fibril structure. Furthermore, the solvation thermodynamic analysis on the simulated protein conformations indicates that $A{\beta}42$ is more hydrophobic than $A{\beta}40$, implying that the surrounding water imparts a larger thermodynamic driving force for the self-assembly of $A{\beta}42$. Taken together, our results provide structural and thermodynamic grounds on why $A{\beta}42$ is more aggregation-prone than $A{\beta}40$ in aqueous environments.

• Animal cells and systems
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• v.4 no.3
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• pp.273-278
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• 2000

Transforming growth factor-$\beta$ (IGF-$\beta$)s are multifunctional small polypeptides synthesized in most cell types. TGF-$\beta$ exerts pivotal effects on both bone formation and resorption. In addition, increasing lines of evidence implicate TGF-$\beta$ as a potential coupling factor between these two processes during bone remodeling. In the present study, the expression form and the activation mechanism of latent-TGF-$\beta$ were investigated using specific antibodies for each isoform. TGF-$\beta$s were observed to be synthesized and accumulated in a large amount in cultured osteoblastic cells. The estimated molecular weights of intracellular TGF-$\beta$2 and -$\beta$3 were 49 and 55 kDa, respectively. Based on proteolytic digestion study and immunofluorescence observation, these precursor forms seemed to be accumulated in distinct intracellular compartments. To examine whether the internal pool of TGF-$\beta$ was possiblely regulated by external signals, their biological activites were examined in a conditioned media of this cell. Although the intact conditioned media did not contain detectable TGF-$\beta$ activity, heat-treatment or acid-activation of the conditioned media revealed significant TGF-$\beta$ activity. Furthermore, in the presence of estrogen, this activity was dramatically diminished. It is known that activation of latent TGF-$\beta$ can be achieved by different chemical and enzymatic treatments, or by incubation with certain cell types. This extracellular activation was suggested as a key step in the regulation of TGF-$\beta$ activity. In addition to these extracellular activation, this study suggests that the synthesis and intracellular processing are important regulation steps for TGF-$\beta$ action. In addition, this regulation Is specific for TGF-$\beta$ type 2, because the change was not observed in TGF-$\beta$3 in osteoblastic cell line.