• 한국산업정보학회논문지
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• 제8권1호
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• pp.43-54
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• 2003

전자상거래는 개인과 개인, 기업과 기업, 개인과 기업 상호간에 메시지의 교환을 통해서 이루어진다. 전자상거래를 활성화 할 수 있는 가장 중요한 요소는 메시지 인증으로서, 이는 거래당사자들이 수신된 메시지의 진정성을 확인하는 과정이다. 메시지의 진정성은 위조불가, 부인불가, 변경불가, 출처인증으로 구성되어 있고, 공개키 암호화를 통해 수행 할 수 있다. X.400 메시지처리 시스템과 공개키 암호화에 기반을 두고 있는 PGP가 메시지 교환에 널리 사용되고 있다. 본 논문에서는 공개키 암호화와 X.400 프로토콜 그리고 PGP상에 존재하는 메시지 인증문제를 해결하기 위하여 NMAP로 명명된 공개정보 기반 암호화 시스템을 제안하고 이를 설계 구현하였다. 구현된 메시지 인증 프로토콜의 검증을 위해 퍼지적분을 사용하였다. 제안된 시스템은 전자상거래의 활성화와 비대화형 인증 서비스 제공에 사용될 수 있을 것이다.

• Archives of Pharmacal Research
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• 제25권5호
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• pp.561-571
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• 2002

The action mechanisms of several chemopreventive agents derived from herbal medicine and edible plants have become attractive issues in cancer research. Tea is the most widely consumed beverage worldwide. Recently, the cancer chemopreventive actions of tea have been intensively investigated. It have been demonstrated that the active principles of tea were attributed to their tea polyphenols. Recently, tremendous progress has been made in elucidating the molecular mechanisms of cancer chemoprevention by tea and tea polyphenols. The suppression of various tumor biomarkers including growth factor receptor tyrosine kinases, cytokine receptor kinases, P13K, phosphatases, ras, raf, MAPK cascades, NㆍFB, IㆍB kinase, PKA, PKB, PKC, c-jun, c-fos, c-myc, cdks, cyclins, and related transducing proteins by tea polyphenols has been studied in our laboratory and others. The IㆍB kinase (IKK) activity in LPS-activated murine macrophages (RAW 264.7 cells) was found to be inhibited by various tea polyphenols including (-) epigallocatechin-3-gallate (EGCG), theaflavin (TF-1), theaflavin-3-gal-late (TF-2) and theaflavin-3,3'-digallate (TF-3). TF-3 inhibited IKK activity in activated macrophages more strongly than did the other tea polyphenols. TF-3 inhibited both IKK1 and IKK2 activity and prevented the degradation of IㆍBㆍand IㆍBㆍin activated macrophage cells. The results suggested that the inhibition of IKK activity by TF-3 and other tea polyphenols could occur by a direct effect on IKKs or on upstream events in the signal transduction pathway. TF-3 and other tea polyphenols blocked phosphorylation of IB from the cytosolic fraction, inhibited NFB activity and inhibited increases in inducible nitric oxide synthase levels in activated macrophage. TF-3 and other tea polyphenols also inhibited strongly the activities of xanthine oxidase, cyclooxygenase, EGF-receptor tyrosine kinase and protein kinase C. These results suggest that TF-3 and other tea polyphenols may exert their cancer chemoprevention through suppressing tumor promotion and inflammation by blocking signal transduction. The mechanisms of this inhibition may be due to the blockade of the mitogenic and differentiating signals through modulating EGFR function, MAPK cascades, NFkB activation as wll as c-myc, c-jun and c-fos expression.

• 대한의생명과학회지
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• 제24권3호
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• pp.213-220
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• 2018

Triglyceride (TG) is known to be associated with inflammatory disease including atherosclerosis. In a variety of atherosclerosis models, T lymphocytes are localized in the earliest lesions of atherosclerosis. T cell associated cytokines such as $TNF-{\alpha}$ and $IFN-{\gamma}$ have pre-dominant inflammatory effects in chronic vascular diseases. In our previous study, we found that the expression of $TNF-{\alpha}$ and its receptor, $TNF-{\alpha}R$ was increased when Jurkat T lymphocyte cell lines were exposed to TGs. Therefore, experiments were conducted to determine which cell signaling pathway are involved in the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs. To identify signal transduction pathways involved in TG-induced upregulation of $TNF-{\alpha}$, we treated TG-exposed Jurkat T cells with specific inhibitors for MEK1, PI3K, $NF-{\kappa}B$ and PKC. We found that inhibition of the MEK1 pathway blocked TG-induced upregulation of $TNF-{\alpha}$. However, the expression level of $TNF-{\alpha}R$ did not change with any signal transduction inhibitor. Based on this observation, we suggest that increase of exogenous TG induces increase of $TNF-{\alpha}$ expression through MEK1 pathway in Jurkat T cells. In addition, it was confirmed that the increase of $TNF-{\alpha}$ and $TNF-{\alpha}R$ expression by TGs occurs via different pathways.

• International Journal of Oral Biology
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• 제42권1호
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• pp.1-8
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• 2017

In the present study, we investigated the role of peripheral ionotropic receptors in artemin-induced thermal hyperalgesia in the orofacial area. Male Sprague-Dawley rats weighting 230 to 280 g were used in the study. Under anesthesia, a polyethylene tube was implanted in the subcutaneous area of the vibrissa pad, which enabled drug-injection. After subcutaneous injection of artemin, changes in air-puff thresholds and head withdrawal latency time were evaluated. Subcutaneous injection of artemin (0.5 or $1{\mu}g$) produced significant thermal hyperalgesia in a dose-dependent manner. However, subcutaneous injection of artemin showed no effect on air-puff thresholds. IRTX ($4{\mu}g$), a TRPV1 receptor antagonist, D-AP5 (40 or $80{\mu}g$), an NMDA receptor antagonist, or NBQX (20 or $40{\mu}g$), an AMPA receptor antagonist, was injected subcutaneously 10 min prior to the artemin injection. Pretreatment with IRTX and D-AP5 significantly inhibited the artemin-induced thermal hyperalgesia. In contrast, pretreatment with both doses of NBQX showed no effect on artemin-induced thermal hyperalgesia. Moreover, pretreatment with H-89, a PKA inhibitor, and chelerythrine, a PKC inhibitor, decreased the artemin-induced thermal hyperalgesia. These results suggested that artemin-induced thermal hyperalgesia is mediated by the sensitized peripheral TRPV1 and NMDA receptor via activation of protein kinases.

• 대한화학회지
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• 제41권4호
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• pp.205-209
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• 1997

신경수초 염기성 단백질(MBP)에 대한 탈인산화의 자리 특이성에 대한 연구를 시험관에서 수행하였다. MBP에서 인산화된 자리를 알아내기 위해서 MBP를 단백질 키나제 C로 인산화 시키고 단백질 탈인산화 효소 PP2A로 탈인산화시켰다. 인산화된 MBP는 트립신으로 잘라내어서 역상 HPLC 크로마토그래피로 펩티드 조각들을 분리하였다. 각 조각들을 섬광 계측한 후 일부 펩티드의 아미노산 서열을 결정하였다. 일곱 개의 방사능을 보이는 펩티드 조각이 검출되었으며 두번째 조각($P_2$)의 $Ser^{55}$에 해당하는 아미노산이 인산화 반응에 가장 큰 민감도를 보였다. 그러나 탈인산화는 다섯번째 고작($P_5$)의 인산이 가장 잘 방출되는 것으로 나타났다. 이 결과는 MBP가 단백질 탈인산화 반응에 적절한 기질임을 보여주고 있다.

• The Korean Journal of Physiology
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• 제29권1호
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• pp.39-50
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• 1995

This study was designed to clarify the action of cyclic nucleotides, cyclic AMP and cyclic GMP, on phorbol 12,13-dibutyrate (PDBu)-induced contraction in rings isolated from rabbit carotid artery. Arterial rings, 2 mm in width, were myographied isometrically in an isolated organ bath. PDBu produced slowly developing, sustained contraction in rabbit carotid artery, in a dose dependent manner, which was independent of extracellular $Ca^{2+}$ PDBu-induced contraction was relaxed by staurosporine, which suggests that PDBu-induced contraction is mediated by protein kinase C (PKC). $^{45}Ca^{2+}$ uptake by rabbit carotid artery was increased by PDBu during depolarization, but not in control. Isoproterenol and sodium nitroprusside (SNP) relaxed phenylephrine-induced contraction. However, SNP but not isoproterenol relaxed the contraction induced by PDBu. Acetylcholine relaxed PDBu-induced contraction in the presence of the endothelium. 8-bromo-cyclic AMP, a permeable analogue of cyclic AMP, suppressed phenylephrine-induced contraction but not PDBu-induced contraction. 8-bromo cyclic GMP relaxed both of them with dose dependency. A large dose of forskolin relaxed PDBu-induced contraction. PDBu increased cyclic AMP without considerable change in the level of cyclic GMP. Based on these findings, PDBu-induced contraction of rabbit carotid artery was relaxed by cyclic GMP more effectively than cyclic AMP, and the action of cyclic AMP could be mediated by cyclic GMP dependent protein kinase. Therefore it is suggested that the antagonistic action between protein kinase C and cyclic GMP-dependent protein kinase plays a major role in the regulation of vascular tone.

• Journal of Microbiology and Biotechnology
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• 제11권5호
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• pp.749-755
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• 2001

High Electromagnetic Field (EMF) with an intensity of 1 mT (Tesla) inhibited the growth of both human normal lung and immune T cell down to $20-30\%$, compared to that of an unexposed case. The human T-cells, Jurkat, were more severely affected by EMF than the human lung cells, which showed a relatively slow cell growth and substantial releas of $Ca^+2$ (3.5 times higher than the human T-cells). However, the growth of hepatoma carcinoma, Hep3B, was enhanced by twice that of an unexposed case. The EMF intensity and exposure time did not affect the growth of the cancer cells very much, while it significantly affected the growth of normal cells. Accordingly, it is possible that EMFs may play a role in the initiation of cancer. The EMFs disturbed the signal transduction and membrane systems, such that a five times higher amount of PKC-${\alpha}$ was released from the cell membrane than in the control. Extended exposure to EMFs, for more than 48 hours, also led to 1 $90\%$ necrotic death pattern from apoptotic cell death. Finally, EMF at an intensity of 1mT with a 24-T exposure promoted the differentiation of HL-60 cells to monocytes/macrophages, possibly causing potential acute leukemia.

• The Korean Journal of Physiology and Pharmacology
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• 제12권1호
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• pp.25-30
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• 2008

Although many studies show that thromboxane $A_2\;(TXA_2)$ has the action of gastrointestinal (GI) motility using GI muscle cells and tissue, there are no reports on the effects of $TXA_2$ on interstitial cells of Cajal (ICC) that function as pacemaker cells in GI tract. So, we studied the modulation of pacemaker activities by $TXA_2$ in ICC with whole cell patch-clamp technique. Externally applied $TXA_2\;(5{\mu}M)$ produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode. The tonic inward currents by $TXA_2$ were inhibited by intracellular application of GDP-${\beta}$-S. The pretreatment of ICC with $Ca^{2+}$ free solution and thapsigargin, a $Ca^{2+}$-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the $TXA_2$-induced tonic inward currents. However, chelerythrine or calphostin C, protein kinase C inhibitors, did not block the $TXA_2$-induced effects on pacemaker currents. These results suggest that $TXA_2$ can regulate intestinal motility through the modulation of ICC pacemaker activities. This modulation of pacemaker activities by $TXA_2$ may occur by the activation of G protein and PKC independent pathway via extra and intracellular $Ca^{2+}$ modulation.

• The Journal of Korean Physical Therapy
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• 제19권4호
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• pp.1-14
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• 2007

Background: It is generally accepted that skeletal muscle contraction is triggered by nerve impulse and intracellular $Ca^{2+}\;([Ca^{2+}]_i)$ released from intracellular $Ca^{2+}$ stores such as sarcoplasmic reticulum (SR). Specifically, this process, called excitation-contraction (E-C) coupling, takes place at intracellular junctions between the plasma membrane, the transverse (T) tubule L-type $Ca^{2+}$ channel (dihydropyridine-sensitive L-rype $Ca^{2+}$ channel, DHPR, also called tetrads), and the SR $Ca^{2+}$ release channel (ryanodine-sensitive $Ca^{2+}$ release channel, RyR, also called feet) of internal $Ca^{2+}$ stores in skeletal muscle cells. Furthermore, it has been reported that the $Ca^{2+-}$ dependent and -independent contraction determine the expression of skeletal muscle genes, thus providing a mechanism for tightly coupling the extent of muscle contraction to regulation of muscle plasticity-related excitation-transcription (E-T) coupling. Purpose: Expression and activity of plasticity-associated enzymes in gastrocnemius muscle strips have not been well studied, however. Methods: Therefore, in this study the expression and phosphorylation of E-C and E-T coupling-related mediators such as protein kinases, ROS(reactive oxygen species)- and apoptosis-related substances, and others in gastrocnemius muscles from rats was examined. Results: I found that expression and activity of MAPKs (mitogen-activated protein kinases, ERK1/2, p38MAPK, and SAPK/JNK), apoptotic proteins (cleaved caspase-3, cytochrome c, Ref-1, Bad), small GTP-binding proteins (RhoA and Cdc42), actin-binding protein (cofilin), PKC (protein kinase C) and $Ca^{2+}$ channel (transient receptor potential channel 6, TRPC6) was observed in rat gastrocnemius muscle strips. Conclusion: These results suggest that MAPKs, ROS- and apoptosis-related enzymes, cytoskeleton-regulated proteins, and $Ca^{2+}$ channel may in part functionally import in E-C and E-T coupling from rat skeletal muscles.

• Asian Pacific Journal of Cancer Prevention
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• 제17권6호
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• pp.2795-2799
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• 2016

Purpose: To study histomorphological and immunohistochemical patterns of gastro-intestinal stromal tumours (GISTs) in Malaysia. Materials and Methods: A total of 29 GIST cases from Hospital Tuanku Ja'afar, Seremban, were studied retrospectively over a period of 10 years from January 2002 to December 2011. Patient demographic data like age, sex and etnicity were collected. Tumour characteristics like site, maximum dimension and specimen type were analysed. Evaluation was according to established criteria into very low, low, intermediate and high-risk categories. Immunohistochemical characteristics were also analysed. Results: The mean age of patients was 59.7 years. Males (59%) were found to be more commonly affected than females (41%). The Chinese (45%) were commonly affected than Malays (41%), and Indians (10%). The most common symptom was pain in the abdomen (13.8%). More than half of the cases were seen in stomach (53%). The tumour size ranged from 1.5 cm to 17 cm with a mean of 6.94cm. Microscopic findings revealed that the spindle cell type was the most common (76%). It was observed that the majority of the cases (48%) were categorised in the intermediate risk group. Immunohistochemical staining showed positivity for CD117 (78.6%), CD34 (71.4%), vimentin (86.2%), S-100 (27.6%), SMA (35.7%), PKC THETA (46.4%) and PDGRFA (67.9%).