• 한국식품영양과학회:학술대회논문집
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• 한국식품영양과학회 2001년도 International Symposium on Food,Nutrition and Health for 21st Century
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• pp.69-73
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• 2001

Two opioid peptides, YPLDL and YPLDLF, were isolated from enzymatic digests of spinach ribulose-1, 5-bisphosphate carboxylase/oxygenase (RuBisCO) and named rubiscolin-5 and -6, respectively. These peptides were selective for delta-receptor and the latter was about 3 times more potent than the former. After oral administration in mice at the dose of 100 mg/kg, rubiscolin-6 showed analgesic activity in tail pinch test. It also stimutated learning performance at the same dose in passive avoidance experiment using step-through apparatus. An immunostimulating peptide, MITLAIPVNKPGR, was isolated from a trypsin digest of soybean protein and named soymetide. Immunostimulating activy of soymetide was mediated by fMLP receptor. Interestingly, after oral administration in rats at a dose of 300 mg/kg (po.), soymetide-4 (MITL) protected alopecia (hair-loss) induced by etoposide, a cancer chemotherapy agent. Stimulation of IL-1 release by the peptide was involved in the mechanism. Ovokinin(2-7), RADHPF, is a vasorelaxing peptide released from ovalbumin by the action of chymotrypsin. It lowered blood pressure of spontaneously hypersensive rats (SHR) after oral administration at a dose of 10 mg/kg. RPLKPW, which was designed by replacing 4 amino acid residues in ovokinin(2-7), exhibited hypotensive activity at a dose of 0.1 mg/kg (po.). This peptides was introduced into 3 homologous sites in soybean beta-conglycinin alpha' subunit by site-directed mutagenesis of the cDNA and expressed in E. coli. The minimum effective dose for hypotensive activity of the genetically modified beta-conglycinin alpha' subunit was 10 mg/kg (po.), which is about 1/200 that of ovalbumin.

• 한국인터넷방송통신학회논문지
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• 제12권1호
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• pp.275-281
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• 2012

커뮤니티 네트워크는 이기종(heterogeneous) 노드들이 시간과 장소에 구애받지 않고 정보를 공유할 수 있는 통신 환경을 말한다. 이를 위해 이동 노드들은 사전에 구성된 통신 인프라 시설에 의존하지 않고 자가 구성될 수 있어야 하고 노드의 이동성으로 인해 변경되는 네트워크 토폴로지에 적응할 수 있어야 한다. 준-인프라 기반 무선 애드-혹 네트워크는 이러한 요구사항을 지원하기에 적합한 통신 기술이다. 본 논문에서는 준-인프라기반 애드-혹 네트워크 프로토콜의 실험에 용이한 평가 도구인 VTC(virtual topology coordinator) 시스템을 제안한다. VTC는 모든 통신장비간 단일 홉 통신만이 가능한 작은 공간에서도 선택적 MAC(Medium Access Control) 프레임 수신 메커니즘을 이용하여 다중 홉 네트워크 토폴로지를 가상으로 구성하도록 해준다. VTC 시스템은 실제의 무선 특성을 모두 반영하기는 어려우나 시뮬레이션을 통한 검증보다는 실 특성을 보다 다양하게 반영시킬 수 있다.

• 미생물학회지
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• 제28권1호
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• pp.19-26
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• 1990

To examine the effects of sequence variations near the transcriptional start site on the rate of formation of the open complexes at bacteriophage $\lambda P_{R}$ promoter, two mutant promoters were created by site-specific mutagenesis using synthetic oligonucleotides. Mutant I coatains changes at positions -3 and -4 from TT to CC, thus having a 6-bp long G/C stretch between -10 region and transciptional start site (+1). Mutant II has changes at positions -5 and -6 from GG to AA, thereby having a 9-bp long A/T stretch between positions -11 and -3. Selective filter binding assays were performed to measure the rate of formation of the open complexes between the wild-type or two mutant $P_{R}$ promoters on 664 bp fragments and E. coli RNA polymerase at two temperatures. At 37.deg.C, the wild-type and two mutants showed similar rates for the formation of open complex. The second order rate constant $k_{a}$ and $\tau _{int}$, as determined from the .tau.-plot analysis, were $(6.0\pm0.4)\times10^{6}M^{-1}sec^{-1}$ and $11\pm5$sec, respectively. At 18.deg.C, however, the wild-type and two mutant promoters showed differences in the kinetic parameters. k for the wild-type promoter was (2.2$\pm$0.1)\times 10^{6}M^{-1}sec^{-1}$ and $\tau _{int}$ was 76$\pm$sec. Mutant I and II exhibited differences mainly in the rate of isomerization ($\tau_{int,I}=91\pm$10 sec, int,II=34$\pm$ sec), whereas the second order rate constant $k_{a}$ was similar to the wild type value. This result implies that at $18^{\circ}C$, the isomerization rate is determined by both protein conformational change and DNA melting, which are separable kinetically according to the 3-step mechanism of Roe et al.(1984,1985), and that the base changes affected mainly the rate of DNA melting as predicted.lting as predicted.

• 한국전산구조공학회논문집
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• 제18권3호
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• pp.311-320
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• 2005

본 논문에서는 평판구조물의 정적 및 동적해석에 사용할 목적으로 성능이 향상된 평판유한요소를 제시하였다. 이 요소는 비적합변위형과 선택적 감차적분방법 그리고 대체전단변형률장을 복합적으로 적용하여 각각의 장점들을 포함하는 향상된 거동을 보여주고 있다. 또한 비적합변위형의 적용으로 발생되는 조각시험의 실패 문제점을 해결하기 위하여 직접수정법을 평판유한요소의 개선에 사용하였다. 대표적인 검증문제에 대한 수치해석작업을 통하여 본 연구에서 개발한 요소는 가상적인 제로에너지모드 및 전단잠김현상의 발생과 같은 문제를 나타내지 않음을 알 수 있었다. 특히 찌그러진 형상으로 모형화 한 경우에 있어서도 전단잠김현상이 발생하지 않았다. 본 연구에서 수행한 동적반응해석 시험에 있어서도 이론해와 잘 일치하는 결과를 보여주었다.

• Journal of Ginseng Research
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• 제39권4호
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• pp.365-370
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• 2015

Background: The beneficial effects of ginsenoside species have been well demonstrated in a number of studies. However, the function of ginsenoside Ro (GRo), an oleanane-type saponin, has not been sufficiently investigated. Thus, the aim of the present study was to investigate the anti-inflammatory effects of GRo in vitro using the Raw 264.7 mouse macrophage cell line treated with lipopolysaccharide (LPS), and to clarify the possible mechanism of GRo involving heme oxygenase-1 (HO-1), which itself plays a critical role in self-defense in the presence of inflammatory stress. Methods: Raw 264.7 cells were pretreated with GRo (up to $200{\mu}M$) for 1 h before treatment with 1 mg/mL LPS, and both cell viability and inflammatory markers involving HO-1 were evaluated. Results: GRo significantly increased cell viability in a dose dependent manner following treatment with LPS, and decreased levels of reactive oxygen species and nitric oxide. GRo decreased inflammatory cytokines such as nitric oxide synthase and cyclooxygenase-2 induced by LPS. Moreover, GRo increased the expression of HO-1 in a dose dependent manner. Cotreatment of GRo with tin protoporphyrin IX, a selective inhibitor of HO-1, not only inhibited upregulation of HO-1 induced by GRo, but also reversed the anti-inflammatory effect of GRo in LPS treated Raw 264.7 cells. Conclusion: GRo induces anti-inflammatory effects following treatment with LPS via upregulation of HO-1.

• 한국자원식물학회지
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• 제28권6호
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• pp.727-733
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• 2015

Although Sophorae Flos (SF) has been reported to exert an anti-cancer activity, molecular targets and mechanisms associated with anti-cancer activity of SF have been unclear. Because cyclin D1 has been regarded as an important regulator in the cell proliferation, we focused cyclin D1 and investigated the effect of SF on the cyclin D1 regulation in light of elucidating the molecular mechanism for SF’s anti-cancer activity. The treatment of SF decreased cellular accumulation of cyclin D1 protein. However, SF did not change the level of cyclin D1 mRNA. Inhibition of proteasomal degradation by MG132 attenuated SF-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with SF. In addition, a point mutation of threonine-286 to alanine attenuated SF-mediated cyclin D1 downregulation. Inhibition of ERK1/2 by a selective inhibitor, PD98059 suppressed cyclin D1 downregulation by SF. From these results, we suggest that SF-mediated cyclin D1 downregulation may result from proteasomal degradation through its threonine-286 phosphorylation via ERK1/2. SF-induced proteasomal degradation of cyclin D1 might inhibit proliferation in human colorectal cancer cells. The current study provides information on molecular events for an anti-cancer activity of SF

• 한국자원식물학회지
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• 제28권6호
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• pp.682-689
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• 2015

Abeliophyllum distichum Nakai (A. distichum) has been reported to exert the inhibitory effect on angiotensin converting enzyme and aldose reductase. Recently, our group found that branch extracts of A. distichum (EAFAD-B) induce apoptosis through ATF3 activation in human colon cancer cells. However, anti-cancer reagents exert their activity through the regulation of various molecular targets. Therefore, the elucidation of potential mechanisms of EAFAD-B for anti-cancer activity may be necessary. To elucidate the potential mechanism of EAFAD-B for anti-cancer activity, we evaluated the regulation of cyclin D1 in human colon cancer cells. EAFAD-B decreased cellular accumulation of cyclin D1 protein. However, cyclin D1 mRNA was not changed by EAFAD-B. Inhibition of proteasomal degradation by MG132 attenuated EAFAD-B-mediated cyclin D1 downregulation and the half-life of cyclin D1 was decreased in the cells treated with EAFAD-B. In addition, EAFAD-B induced cyclin D1 phosphorylation at threonine-286 and the point mutation of threonine-286 to alanine attenuated EAFAD-B-mediated cyclin D1 proteasomal degradation. Inhibitions of both ERK1/2 by PD98059 and NF-κB by a selective inhibitor, BAY 11-7082 suppressed cyclin D1 downregulation by EAFAD-B. From these results, we suggest that EAFAD-B-mediated cyclin D1 downregulation may result from proteasomal degradation through its threonine-286 phosphorylation via ERK1/2-dependent NF-κB activation. The current study provides new mechanistic link between EAFAD-B and anti-cancer activity in human colon cancer cells.

• 약학회지
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• 제43권1호
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• pp.33-41
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• 1999

Whereas as selective inhibitor of monoamine oxidase type B, ${\ell}-deprenyl$ (selegiline), is now widely used in the treatment of Parkinson's disease, the precise action mechanism of the drug remains elusive. In this study, to investigate protective effect of ${\ell}-deprenyl$ against the dopamine depletion induced by 6-hydroxydopamine (6-OHDA), the changes in tissue contents of dopamine, serotonine (5-HT) and their metabolites by ${\ell}-deprenyl$ were examined in intact and 6-OHDA-lesioned rat brain. In intact rats, a single intraperitoneal (i.p.) administration of ${\ell}-deprenyl$ showed a no change in striatal dopamine and its metabolites at low concentrations (0.25 and 1 mg/kg), but significantly inhibited dopamine metabolism at a higher concentration (10 mg/kg). The repeated administration of ${\ell}-deprenyl$ (0.25 and 1 mg/kg, i.p., for 21 consecutive days) reduced the contents of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanilic acid (HVA) in dose-dependent manners without changes in dopamine content. Bilateral intracerebroventricular (i.c.v) infusion of 6-OHDA ($100{\;}\mu\textrm{g}/10{\;}{\mu}{\ell}/hemisphere$) depleted dopamine in striatum and septum by 81% and 90% respectively. When rats were pretreated with ${\ell}-deprenyl$ before 6-OHDA administration, the striatal and septal dopamine levels were significantly increased by about 3.0-fold and 3.4-fold, respectively, compared to the untreated 6-OHDA-lesioned rat. Pretreatment of ${\ell}-deprenyl$ also significantly enhanced the dopmaine metabolites, DOPAC, HVA and 3-methoxytyramine, in the striatum, and DOPAC in the septum. These results indicate that a ${\ell}-deprenyl$ pretreatment prevents 6-OHDA-induced depletion of striatal dopamine and its metabolites.

• International Journal of Oral Biology
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• 제43권1호
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• pp.43-51
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• 2018

$K^+$ channels are key components of the primary and secondary basolateral $Cl^-$ pump systems, which are important for secretion from the salivary glands. Paroxetine is a selective serotonin reuptake inhibitor (SSRI) for psychiatric disorders that can induce QT prolongation, which may lead to torsades de pointes. We studied the effects of paroxetine on a human $K^+$ channel, human ether-a-go-go-related gene (hERG), expressed in Xenopus oocytes and on action potential in guinea pig ventricular myocytes. The hERG encodes the pore-forming subunits of the rapidly-activating delayed rectifier $K^+$ channel ($I_{Kr}$) in the heart. Mutations in hERG reduce $I_{Kr}$ and cause type 2 long QT syndrome (LQT2), a disorder that predisposes individuals to life-threatening arrhythmias. Paroxetine induced concentration-dependent decreases in the current amplitude at the end of the voltage steps and hERG tail currents. The inhibition was concentration-dependent and time-dependent, but voltage-independent during each voltage pulse. In guinea pig ventricular myocytes held at $36^{\circ}C$, treatment with $0.4{\mu}M$ paroxetine for 5 min decreased the action potential duration at 90% of repolarization ($APD_{90}$) by 4.3%. Our results suggest that paroxetine is a blocker of the hERG channels, providing a molecular mechanism for the arrhythmogenic side effects of clinical administration of paroxetine.

• 대한전자공학회논문지TC
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• 제43권12호
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• pp.61-67
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• 2006

본 논문에서는 고속무선통신에 널리 사용되고 있는 직교 주파수 분할 다중화 데이터 전송시스템에서 반송파주파수 옵셋(Offset)에 의한 잔류 위상 오차와 샘플링 주파수 옵셋에 의한 잔류 오차를 추적하고 보상하는 알고리즘을 제안한다. 직교 주파수 분할 다중화 시스템에서는 서로 직교성을 가지는 부반송파들이 디지털 데이터에 의해 변조되어 동시에 전송된다 반송파 주파수 옵셋이 존재하는 경우에는 신호 대 잡음비의 감소 그리고 인접 부반송파의 간섭 등이 발생한다. 또한 송신단과 수신단에서의 샘플링 주파수의 차이로 인한 샘플링 시점의 오차도 직교 주파수 분할 다중화 시스템에서 성능저하의 주요한 요인으로 작용한다. 반송파 주파수의 오차와 샘플링 주파수의 오차는 직교 주파수 분할 다중화 시스템에서 중요한 성질중의 하나인 직교성 상실을 초래하며 이는 성능저하의 원인으로 작용하므로 수신단에서는 지속적으로 잔류 오차를 추적하여 보상해 주는 방식의 적용이 필수적이다. 본 논문에서는 주파수 선택적 페이딩 무선 채널 환경에서 파일롯 데이터뿐만 아니라 채널이득 정보 및 페이로드 데이터를 주파수 오차 추정에 반영하여 추정오차를 줄이고 이 추정 값을 주파수 오차 보상에 반영하여 성능 향상을 달성할 수 있는 방식을 제안한다.