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      • 위장관의 원발성 B 세포 악성 림프종의 재분류와 bcl-2, cyclin D1, bcl-6 및 p53 발현의 의미

        서정균,김태원,김병수,조은택,박찬국,김만우,이미자,전호종 조선대학교 2001 The Medical Journal of Chosun University Vol.26 No.2

        Background and Objectives : In recent years, the REAL (Revised European American Lymphoma) classification provided a new category of MALT (mucosa-associated lymphoid tissue) lymphoma and mantle cell lymphoma in B cell lymphomas. We have analyzed the expression of bcl-2, cyclin D1, bcl-6 and p53 and correlated with the subtypes and histologic grade of primary gastrointestinal B cell lymphoma. Also we investigated the usefulness of immunophenotypic features in diagnosis of low grade B cell lymphoma. Materials and Methods : Twenty-two cases of primary gastrointestinal B cell lymphoma were recategorized in low grade MALT lymphoma, low/high grade MALT lymphoma, high grade MALT lymphoma, and diffuse large cell lymphoma according to the morphological findings. We investigated the expression of bcl-2, cyclin D1, bcl-6 and p53 by immunohistochemical method. Results : The bcl-2 protein expression was higher in the low grade MALT lymphoma than in the high grade lymphoma. The cyclin D1 protein expression was negative in all cases. The expression of bcl-6 and p53 protein was negative in all low grade MALT lymphoma. Conclusion : The results suggest that we can differentiate the low grade lymphoma from the high grade lymphoma by immunohistochemical staining for bcl-2, bcl-6, and p53 protien.

      • KCI등재

        Amylase가 Hydroxyapatite 탈회에 미치는 영향

        서정택,이인환,최병재,이종갑 大韓小兒齒科學會 1998 大韓小兒齒科學會誌 Vol.25 No.2

        Salivary proteins which are produced in the saliary acinar cells have been known to be involved in the Calcium and phosphate metabolism. The acquired pellicle resulting from such metabolism is considered as a secondary defence membrane against tooth caries. In this respect, some proteins included in saliva probably play an important role in the prevention of demineralization in enamel. On the other hand, fluoride has long been known to prevent the demineralization of enamel by the inhibition of the growth of Streptococcus mutans (S.mutans) and by the chemical reaction with calcium and phosphate. therefore, I have examined the roles of amylase and albumin in the demineralization of enamel and compared these preteins with fluoride in terms of anticariogenic effect. 1. The demineralization caused by S. mutans occurred slowly and progressively for the first 60 min, then the rate of demineralization was accelerated afterwards. 2. pH decreased continuously during the entire period of each experiment. 3. the demineralization was significantly inhibited by the preteatment of amylase and fluoride but albumin had little effect on it. 4. An addition of 0.1 mM lactic acid (final concentration 0.1μM) caused a rapid increase in calcium concentration reaching a mazimum within 10 min. 5. pH decreased rapidly by the addition of 0.1mM lactic acid and reached a minimum within a few seconds followed by an increase in pH. pH reaced a plateu with 10 min. 6. Fluoride, amylase and albumin played little role in the 0.1 mM lactic acid-induced demineralization. 7. A slow infusion of 0.1 M lactic acid at a rate of 5 ㎕/min caused a slower increased I calcium concentration compared with the bolus addition of lactic acid. 8. Fluoride had an inhibitory effect on the calcium release caused by slow infusion of lactic acid while amylase and albumin had no effect on it. These results suggest that fluoride inhibits demineralization by protecting the HA from the acid attack whereas amylase has a direct effect on S. mutans to prevent demineralization.

      • KCI등재

        Na+/H+ exchanger와 HCO-₃Transporter에 의한 흰쥐 타액선 선세포내 pH 조절

        서정택,박동범,손흥규,이종갑 大韓小兒齒科學會 1998 大韓小兒齒科學會誌 Vol.25 No.2

        Intracellular pH (pHi) plays an important role in the regulation of cellular processes by influencing the activity of various enzymes in cells. Therefore, almost every type of mammalian cell possesses an ability to regulate its pHi. One of the most prominent mechanisms in the regulation of pHi is Na+/H+ exchanger. This exchanger has been known to be activated when cells are stimulated by the binding of agonist to the muscarinic receptors. Therefore, the aims of this study were to compare the rates of H+ extrusion through Na+/H+ exchanger before and during muscarinic stimulation and to investigate the possible existence of HCO-₃ transporter which is responsible for the continuous supply of HCO-₃ ion to saliva. Acinar cells were isolated from the rat mandibular salivary glands and loaded with pH-sensitive fluoroprobe, 2', 7' -bis(2-carboxyethyl)-5(6)-carboxyfluorescein(BCECF), for 30min at room temperature. Cells were attached onto the coverglass in the perfusion chamber and the changes in pHi were measured on the iverted microscope using spectrofluormeter. 1. By switching the perfusate from HCO-₃-free to HCO-₃-buffered solution, pHi decreased by 0.39±0.02 pH units followed by a slow increase at an initial rate of 0.04±0.007 pH units/min. the rate of pHi increase was reduced to 0.01±0.002 pH units/min by the simultaneous addition of 1 mM amilorede and 100μM DIDS. 2. An addition and removal of NH+₄ caused a decrease in pHi which was followed by an increase in pHi. The increase of pHi was almost completely blocked by 1mM amiloride in HCO-₃-free perfusate which implied that the pHi increase was entired dependent on the activation of Na+/H+ exchanger in HCO-₃=free condition. 3. An addition of 10μM carbachol increased the initial rate of pHi recovery from 0.16±0.01 pH units/min to 0.28±0.03pH units/min. 4. The initial rate of pHi decrease induced by 1mM amilorede was also increased by the exposure of the acinar cells 10μM carbachol(0.06±0.008pH unit/min) compared with that obtained before carbachol sitmulation (0.03±0.004pH unit/min). 5. The intracellular buffering capacity β1 was 14.31±1.82 at pHi 7.2-7.4 and β1 increased as pHi decreased. 6. The rate of H+ extrusion through Na+/H+ exchanger was greatly enhanced by the stimulation of the cells with 10μM carbachol and there was an alkaline shift in the activity of the exchanger. 7. An intrusion mechanism of HCO-₃ was identified in rat mandibular salivary acinar cells. Taken all together, I observed 3-ford increased in Na+/H+ exchanger by the stimulation of the acinar cells with 10μM carbachol at pH 7.25. In addition, I have found an additional mechanism for the regulation of pHi which transported HCO-₃ into the cells.

      • W^(sh)/W^(sh) 마우스 고환에서 Protein Kinase C(PKC)와 c-kit의 발현 양상

        곽현정,최병민,서기석,임정식,정헌택 大韓免疫學會 1996 大韓免疫學會誌 Vol.18 No.3

        Protein kinase C (PKC) is a multigene family of at least nine serine/threonine kinases that are central to many signal transduction pathways. And the expression of PKC gene is strictly con-trolled by developmental stage. Mutation of the W (c kit) gene, which encodes a transmembrane tyrosine kinase receptor, affect the development and differentiation stem cells. Most homozygous W mutant mice are sterile, due to a lack of germ cells arising during embryonic development, but one of notable exception is W */Wh mice, which are fully fertile in both sexes. In order to elucidate the biological functions of PKC S and c-kit in the testes, we have examined the expression of PKC b mRNA and c-kit mRNA in While mouse testes by means of Northern blotting. North-em blot results was demonstrated that only PKC 8, 4, 8 mRNA can be detected in normal mouse testes. PKC, 8 mRNA was weakly expressed in 7 and 8-week-old mice and highly ex-pressed by 12 weeks. The PKC 8 mRNA and the c-kit mRNA was detectable in the testes of Whl Wh mouse. These results indicated that the function of the PKC a gene is necessary for the development and the W (c-kit) gene is important for the transmission of signal in testes.

      • KCI등재

        흰쥐 악하선 세포에서 gap junction 봉쇄제인 octanol이 타액분비 및 세포내 Ca²+ 농도 조절에 미치는 영향

        이승일,서정택,이종갑,이주석,손흥규 大韓小兒齒科學會 1999 大韓小兒齒科學會誌 Vol.26 No.2

        세포내 유리칼슘(free calcium. Ca²+)은 세균에서 고등동물에 이르기까지 거의 모든 세포에서 세포 고유작용을 조절하는 중요한 세포내 신호전달체계(signal transduction system)의 매개체이다. 타액선 세포에서 부교감 신경 자극으로 타액분비가 증가될 때에도 세포내 Ca²+ 농도 증가가 가장 중요한 역할을 한다. 그러나 췌장(pancreas)의 경우 세포내 Ca²+ 이외에도 인접세포를 전기적, 화학적으로 연결해주는 gap junction이 외분비 기능을 직접적으로 조절할 가능설이 제시되었다. 타액선 세포에서도 세포막에 고농도의 gap junction이 존재하고 있으며, gap junction을 통해 인접세포들이 전기적, 화학적으로 연계되어 있어 gap junction이 타액선 세포의 기능을 직접적으로 조절할 가능성을 내포하고 있다. 따라서 gap junction이 타액선의 타액분비 작용에도 중요한 역할을 하며 이러한 작용이 세포내Ca²+ 농도를 조절하여 이루어질 것이라는 가정하에 이를 확인하는 실험을 시행하였다. 흰쥐 악하선에서 유리되는 타액양을 측정하기 위해서 악하선으로 혈액을 공급하는 동맥에 가는 관을 삽입하여 생리 식염수를 관류하면서 타액선관을 통해 타액을 채취하였다. 세포내Ca²+ 농도는 분리한 악하선 acini 내에Ca²+ 농도 변화에 민감하게 반응하는 형광물질인 fura-2를 축적시키고 형광 분석기를 사용하여 형광강도를 측정하여 다음과 같은 결과를 얻었다. 1. CCh 투여로 타액 분비가 증가하였을 때 gap junction을 봉쇄하는 약물인 octanol(1 mM)을 투여하면 타액분비가 봉쇄되었으며 이는 가역적 반응이었다. 2. CCh 투여로 세포내 Ca²+ 농도가 증가하였을 때 1mM octanol을 투여하면 세포내 Ca²+농 도가 CCh 투여전의 상태로 감소되었다. 3. Octanol은 CCh에 의하여 유발된 초기Ca²+ 증가를 억제하지는 못한 반면에 후기 vvvvv 농도를 감소시켰다. 4. 세포막 Ca²+ 통로를 열어주는 약물인 thapsigarain(1μM)을 투여하여 세포내Ca²+ 농도를 증가시킨 후 1mM octanol을 투여하면 세포내 Ca²+ 농도가 thapsigarain 투여 전의 상태로 감소하였다. 5. 2,5-di-tert-butyl-1, 4-benzohydroquinone (TBQ)의 투여로 세포막을 통한 Ca²+농도의 주기적 변동인Ca²+ 의 oscillation이 유발되었는데, 이때 1mM octanol을 투여한 경우에 Ca²+ 농도의 oscillation이 정지하여 역시 gap juncion을 봉쇄하면 TBQ에 의해서 유발된 세포내 Ca²+ 농도의 주기적 변동이 사라지고 Ca²+ 농도의 감소가 나타남을 확인하였다. 6. Gap junction을 봉쇄하는 또 다른 약물인 glycyrrhetinic acid(100μM)도 CCh 자극으로 인한 타액분비를 억제하였다. 이상의 결과로 미루어 gap junction은 흰쥐 악하선 세포로부터의 타액분비 조절에 중요한 역할을 하는 이는 gap junction이 세포막 Ca²+ 통로를 조절함으로써 수용체 자극으로 유발된 세포내 농도 변화에 영향을 미친 결과인 것으로 추측된다. From bacteria to mammalian cells, one of the most important mediators of intracellular signal transduction mechanisms which regulate a variety of intracellular processes is free calcium. In salivary acinar cells, elevation of intracellular calcium concentration ( 〔Ca²+〕 ) is essential for the salivary secretion induced by parasympathetic stimulation. However, in addition to〔Ca²+〕, gap junctions which couple individual cells electrically and chemically have also been reported to regulate enzyme secretion in pancreatic acinar cells. Since the plasma membrane of salivary acinar cells has a high density of gap junctions, and these cells are electrically and chemically coupled with each other, gap junctions may modulate the secretory function of salivary glands. In this reapect, I planned to investigate the role of gap junctions in the modulation of salivary secretion and 〔Ca²+〕 using mandibular salivary glands of rats. In order to measure the salivary flow rate, fluid was collected from the cannulated duct of the isolated perfused rat mandibular glands at 2 min intervals.〔Ca²+〕 was measured form the cells loaded with fura-2 by spectrofluorometry. The results obtained were as follows : 1. CCh-induced salivary secretion was reversibly inhibited by 1 mM octanol, a gap junction blocker. 2. CCh-induced increase in 〔Ca²+ 〕was also reversed by the applocation of 1 mM octanol. 3. Octanol did not block the initial increase in 〔Ca²+〕 caused by CCh, which suggested that the reduction of〔Ca²+〕 caused by gap junction blockade was not resulted from the inhibition of Ca²+ release from intracellular Ca²+ stores. 4. Addition of octanol during stimulation with 1μM thapsigargin, a potent microsomal ATPase inhibitor, reduced 〔Ca²+ 〕to the basal level. This suggested that inhibition of gap junction permeability closed plasma membrane Ca²+ channels. 5. 2,5-di-tert-butyl-1, 4-benzohydroquinone (TBQ) generated 〔Ca²+ 〕oscillations resulting from periodic influx of Ca²+ via plasma membrane. The TBQ-induced〔Ca²+ 〕 oscillations were stopped by the application of 1mM octanol which implicated that gap junctions modulate the permeability of plasma membrane Ca²+ channels. 6. Glycyrrhetinic acid, another well known gap junction blocker, also inhibited CCh-induced salivary secretion from rat mandibular glands. These results suggested that gap junctions play an important role in the modulation of fluid secretion from the fat mandibular glands and this was probably due to the inhibition ofCa²+ influx through the plasma membrane Ca²+ channels.

      • KCI등재

        소아의 다발성 치아우식증과 연관된 타액의 생화학적 특성

        이승일,장희순,조우성,최병재,서정택 大韓小兒齒科學會 1998 大韓小兒齒科學會誌 Vol.25 No.4

        Saliva is obviously potential medium to protect the dental caries by not only physical clearing effect, but aggregatiog action of protein with bacteria. Nevertheless, we still do not understand how the dental caries occur and what brings the individual difference in caries prevalence. In the regards of dental caries prevalence, we hypothesized that the composition of salivary protein might be different from caries susceptible group to caries resistant group. The purposes of this experiment were focused on the molecular analysis of salivary proteins from the subjects who were involved in multiple caries. Electrophoretic analysis was eone on the whole saliva collected from the children with and without multiple caries. We found 86.2% of subjects with multiple caries has approximately 120 KDa protein band while 30.4% in the healthy subjemts. And the concentration of the total protein on the subjects with multiple caries is significantly higher than that of the healthy group. However, it turned out that the difference of the salivary composition does vot affect the bacterial adhesion to hydroxyapatite bead. With regards of enzymes in salva, the activity of α-amylase and lactate dehydrogenase does not have any significant difference between both groups. However, the concentrations of Na+ and Cl- in saliva from multiple caries group is higher than that of the control group. Taken all together, it may be concluded that 120 KDa protein in saliva may be associated with the process of dental caries, also the high concentration of protein and Na+, Cl- in saliva may be linked to dental caries development as a cofactors.

      • KCI등재후보

        Caffeine Inhibits Acetylcholine- and Noradrenaline-Evoked but not Substance P-Evoked Intracellular Ca^2+ increases in Rat Mandibular Salivary Acini

        Seo, Jeong Taeg,Lee, Syng Ill,Steward, Martin C.,Elliott, Austin C. The Official Publication of Korean Academy of Oral 1995 International Journal of Oral Biology Vol.19 No.2

        The inhibitory effects of caffeine on the increases in intracellular Ca^2+ concentration ([Ca^2+]_i) induced by muscarinic, α-adrenergic and substance-P (SP) receptor stimulations were investigated in mandibular salivary acini isoloted from the rats. The acini loaded with fura-2 were exposed to excitation wavelength at 340 and 380 nm. The emitted fluorescence was measured at 510 nm with a photomultiplier tube attached to the spectrofluorometer system. The acini were first stimulated with 1 μM acetylcholine (ACh) followed by the second stimulation with ACh, noradrenaline or SP and the data were normalized by setting the first peak values of [Ca^2+]_i increases to 100%. The peak value of [Ca^2+]_i increase caused by the second stimulation with 1 μM ACh was reduced to 79.4±3.4% (n=7) compared with the first. In the presence of 20 mM caffeine, the second peak value of [Ca^2+]_i increase was reduced to 23.4±3.0% (n=7, p<0.001). The increase in [Ca^2+]_i caused by 3 μM noradrenaline stimulation was also greatly inhibited by the pretreatment with caffeine. In contrast. 5 nM SP-induced [Ca^2+]_i increase was reduced from 103.8±7.2%(n=8) to 87.2±4.6%(n=10) by the pretreatment with 20 mM caffeine but this difference was not significant. When the acini were subsequently stimulated with ACh and SP in the absence of perfusate Ca^2+,[Ca^2+]_i increase in response to SP was completely abolished(n=3). This result suggests that ACh and SP mobilize Ca^2+ from the same intracellular Ca^2+ pool. In conclusion, caffeine does not block the SP-induced [Ca^2+]_i increase while the ACh- and noradrenaline-induced[Ca^2+]_i increases were inhibited by caffeine. Since these two receptors both activate the common signalling pathway leading from G-protein to [Ca^2+]_i increase, the most possible site of caffeine action is receptor-G protein interaction.

      • SCISCIESCOPUS

        Activation of Rac1-dependent redox signaling is critically involved in staurosporine-induced neurite outgrowth in PC12 cells

        Kim, Du Sik,An, Jeong Mi,Lee, Han Gil,Seo, Su Ryeon,Kim, Seon Sook,Kim, Ju Yeon,Kang, Jeong Wan,Bae, Yun Soo,Seo, Jeong Taeg Informa Healthcare 2013 Free radical research Vol.47 No.2

        <P>Staurosporine, a non-specific protein kinase inhibitor, has been shown to induce neurite outgrowth in PC12 cells, but the mechanism by which staurosporine induces neurite outgrowth is still obscure. In the present study, we investigated whether the activation of Rac1 was responsible for the neurite outgrowth triggered by staurosporine. Staurosporine caused rapid neurite outgrowth independent of the ERK signaling pathways. In contrast, neurite outgrowth in response to staurosporine was accompanied by activation of Rac1, and the Rac1 inhibitor NSC23766 attenuated the staurosporine-induced neurite outgrowth in a concentration-dependent manner. In addition, suppression of Rac1 activity by expression of the dominant negative mutant Rac1N17 also blocked the staurosporine-induced morphological differentiation of PC12 cells. Staurosporine caused an activation of NADPH oxidase and increased the production of reactive oxygen species (ROS), which was prevented by NSC23766 and diphenyleneiodonium (DPI), an NADPH oxidase inhibitor. Staurosporine-induced neurite outgrowth was attenuated by pretreatment with DPI and exogenous addition of sublethal concentration of H<SUB>2</SUB>O<SUB>2</SUB> accelerated neurite outgrowth triggered by staurosporine. These results indicate that activation of Rac1, which leads to ROS generation, is required for neurite outgrowth induced by staurosporine in PC12 cells.</P>

      • KCI등재후보

        Hypertonicity Down-regulates the 1α,25(OH)₂Vitamin D₃-induced Osteoclastogenesis Via the Modulation of RANKL Expression in Osteoblast

        Jeong, Hyun-Joo,Yushun, Tian,Kim, Bohye,Nam, Mi-Young,Lee, Hyun-A,Yoo, Yun-Jung,Seo, Jeong-Taeg,Shin, Dong-Min,Ohk, Seung-Ho,Lee, Syng-Ill Korean Academy of Oral Biology and the UCLA Dental 2005 International Journal of Oral Biology Vol.30 No.1

        Bone remodeling is a process controlled by the action of two major bone cells; the bone forming osteoblast and the bone resorbing osteoclast. In the process of osteoclastogenesis, stromal cells and osteoblast produce RANKL, OPG, and MCSF, which in turn regulate the osteoclastogenesis. During the bone resorption by activated osteoclasts, extra cellular Ca^(2+)/PO^(2-)₄ concentration and degraded organic materials goes up, providing the hypertonic microenvironment. In this study, we tested the effects of hypertonicity due to the degraded organic materials on osteoclastogenesis in co-culture system. It was examined the cellular response of osteoblastic cell in terms of osteoclastogenesis by applying the sucrose, and mannitol, as a substitute of degraded organic materials to co-culture system. Apart from the sucrose, mannitol, and NaCl was tested to be compared to the effect of organic osmotic particles. The addition of sucrose and mannitol (25, 50, 100, 150, or 200mM) to coculture medium inhibited the number of tartrate-resistant acid phosphatase (TRAP) positive multinucleated cells induced by 10nM lα, 25(OH)₂vitaminD₃ (lα, 25(OH)₂D₃). However, NaCl did exert harmful effect upon the cells in this co-culture system, which is attributed to DNA damage in high concentration of NaCl. To further investigate the mechanism by which hypertonicity inhibits lα, 25(OH)₂D₃induced osteoclastogenesis, the mRNA expressions of receptor activator of nuclear factor (NF)-kB ligand (RANKL) and osteoprotegerin (OPG) were monitored by RT-PCR. In the presence of sucrose (50mM), RANKL mRNA expression was decreased in a dose-dependent manner, while the change in OPG and M-CSF mRNA were not occurred in significantly. The RANKL mRNA expression was inhibited for 48 hours in the presence of sucrose (50mM), but such a decrement recovered after 72 hours. However, there were no considerable changes in the expression of OPG and M-CSF mRNA. Conclusively, these findings strongly suggest that hypertonic stress down-regulates lα, 25(OH)₂D₃-induced osteoclastogenesis via RANKL signal pathway in osteoblastic cell, and may play a pivotal role as a regulator that modulates osteoclastogenesis.

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