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급성 췌장염 환자에서 양성자펌프억제제의 효과-예비 연구
유정환 ( Jeong Hwan Yoo ),권창일 ( Chang Ii Kwon ),유광호 ( Kwang Ho Yoo ),윤해리 ( Har Ry Yoon ),김원희 ( Won Hee Kim ),고광현 ( Kwang Hyun Ko ),홍성표 ( Sung Pyo Hong ),박필원 ( Pil Won Park ) 대한소화기학회 2012 대한소화기학회지 Vol.60 No.6
목적: 급성 췌장염의 발생에는 다양한 기전이 관여하고 있고 활성산소가 중요한 역할을 한다고 알려져 있다. 널리 사용되고 있는 양성자펌프억제제인 pantoprazole은 췌장의 소화효소의 분비를 간접적으로 억제하는 작용 외에도 활성산소에 대한 항산화효과와 항염증효과를 가지고 있다. 이번 연구는 이런 pantoprazole의 사용이 급성 췌장염의 임상 경과에 어떤 영향을 미치는지 알아보고자 하였다. 대상 및 방법: 2011년 3월부터 2012년 5월까지 급성 췌장염으로 입원한 환자 중 위식도 역류질환이 동반된 40명을 대상으로 전향적 무작위 배정으로 연구하였다. 20명씩 두 군으로 나누어 한 군에서는 pantoprazole을 투여하였고 다른 군에서는 사용하지 않았다. Pantoprazole은 금식기간 동안에는 하루 2번 40 mg을 정맥 내로 투여하였고 식사 시작 후에는 하루 2번 40 mg을 퇴원할 때까지 경구 투여하였다. 다른 급성 췌장염의 치료는 양 군에서 동일하게 사용되었다. 혈청 amylase, lipase 등의 혈액학적 검사와 APACHE II 점수를 연속적으로 측정하였고 입원 당시 복부 전산화단 층촬영을 시행하여 CT 중증도 지수를 측정하였다. 결과: 양 군 간에 기준 특성, 혈액검사, APACHE II 점수, CT 중증도 지수에서 유의한 차이를 보이지 않았다. Pantoprazole 투여군에서 평균 입원일은 7.4일, 경구 섭취까지 걸린 시간은 69.0시간, 복통이 호전될 때까지 걸린 시간은 59.7시간이었다. APACHE II 점수는 입원 당시에는 3.15이었고 퇴원 시에는 2.35이었다. Pantoprazole을 투여하지 않은 군에서는 평균 입원일은 7.6일, 경구 섭취까지 걸린 시간은 71.4시간, 복통이 호전될 때까지 걸린 시간은 61.8시간이었다. APACHE II 점수는 입원 당시에는 4.4이었고 퇴원 시에는 2.85이었다. 모두 양 군에서 통계학적으로 유의한 차이를 보이지 않았다. 결론: Pantoprazole을 이용한 치료가 급성 췌장염의 경과에 어떤 개선도 보이지 못했다. 그러나 예비 연구라는 점을 고려했을 때, 더 큰 규모의 전향적 무작위 배정 임상연구로 검증이 필요하겠다. Background/Aims: Oxygen free radicals play an important role in acute pancreatitis. Pantoprazole as a proton pump inhibitor (PPI) has pancreatic anti-secretory effect and a pronounced inhibitory reactivity towards hydroxyl radicals. The objective of the study was to investigate the effect of pantoprazole on the course of acute pancreatitis. Methods: We conducted a prospective randomized trial involving 40 patients with acute pancreatitis. Patients were divided into two groups. One group received PPI and the other group did not receive PPI. In the PPI group, patients received pantoprazole 40 mg intravenously twice a day for fasting time, and then 40 mg orally twice a day until discharge. Results: There were no significant differences in baseline characteristics and laboratory markers between two groups. In the pantoprazole group, mean hospital stay was 7.4 days, time to start oral intake was 69.0 hours, and time to pain relief was 59.7 hours. Acute physiology and chronic health evaluation (APACHE) II score was 3.15 at admission day and 2.35 at discharge. On the other hand, in the non-pantoprazole group, mean hospital stay was 7.6 days, time taken to start oral intake was 71.4 hours, and time taken to pain relief was 61.8 hours. APACHE II score was 4.4 at admission and 2.85 at discharge. However, there were no significant differences between two groups. Conclusions: Treatment with pantoprazole did not have influence on the clinical course of acute pancreatitis. But, considering it was a pilot study, large scale prospective trials will be needed.
Differential regulation of tyrosine hydroxylase expression by sonic hedgehog
Kwon, II Sun,Park, Rae Hee,Choi, Jung Mi,Kim, Seung U.,Lee, Young Don,Suh-Kim, Haeyoung Lippincott Williams Wilkins, Inc. 2006 NEUROREPORT - Vol.17 No.7
Sonic hedgehog functions to induce floor plate in early stages, and spinal motor neurons and midbrain dopaminergic neurons in later stages of development. Here, we investigated the effects of sonic hedgehog on tyrosine hydroxylase expression in three cell lines that correspond to different stages of neural development. Sonic hedgehog increased the tyrosine hydroxylase gene expression in pluripotent P19 cells but repressed it in tyrosine hydroxylase-producing PC12 cells. Promoter analysis in mouse neural stem cells indicated that the N-terminal of sonic hedgehog repressed both the basal and cAMP-dependent protein kinase A-mediated tyrosine hydroxylase activity. These results suggest that the N-terminal of sonic hedgehog increases tyrosine hydroxylase gene expression in cells to acquire dopaminergic phenotypes, but decreases expression in late born neurons by antagonizing the protein kinase A cAMP-responsive element binding protein pathway.
( Ii Ho Yang ),( Dong Yun Chae ),( Sung Man Lim ),( Su Kwon Kwon ),( Eun Ae Kim ),( Jae Keun Lim ) 한국과학교육학회 2012 한국과학교육학회지 Vol.32 No.3
This study introduces the development of elementary science textbooks in Korea, In Korea there has been eight revisions to the National curriculum and the development of nine textbooks. The State of Korea has organized textbook development teams, but this time the State chose the development team through public contest. Researchers suggested the ``FLOW`` development model based upon results of studies in creative education and developed the new science textbooks. The ``FLOW`` model includes four stages, aimed towards capturing students`` interest in science (Fun Science), engaging students in various scientific inquiries and experiences (Lab. Experience), organizing their own knowledge of science (Organizing Knowledge), and to encourage students to become little scientists (Willing to be a Scientist). The textbook is a research-developmental textbook that utilizes various literature and exploration-strategic textbooks. The textbook`s basis is formed upon scientists` experiences that assist in the realization of ``inquiry`` that is emphasized within the science field.
Kwon, Ii-Seul,Kwak, Jong Hwan,Pyo, Suhkneung,Lee, Hee-Weon,Kim, AeRyon,Schmitz, Francis J. American Chemical Society and American Society of 2017 Journal of natural products Vol.80 No.1
<P>A new anthranilic acid derivative (1) was isolated from a Philippine sponge, Oscarella stillans (Bergquist and Kelly). The structure of compound 1, named oscarellin, was determined as 2-amino-3-(3'-aminopropoxy)benzoic acid from spectroscopic data and confirmed by synthesis. We examined the immunomodulating effect of compound 1 and its mechanism in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Our data indicated that the expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 were significantly reduced by the pretreatment of 1 (0.1-10 mu M) for 2 h. In addition, compound 1 suppressed activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun NH2-termimal kinase (JNK), but not p38 mitogen-activated protein kinase (MAPK) in LPS-stimulated RAW 264.7 cells. Compound 1 abrogated LPS-induced nuclear factor-kappa B (NF-kappa B) and activator protein-1 (AP-1) activities, whereas the induction of activating transcription factor-3 (ATF-3) was increased. Taken together, our results suggest that compound 1 attenuates pro-inflammatory cytokines via the suppression of JNK, ERK, AP-1, and NF-kappa B and the activation of the ATF-3 signaling pathway.</P>
A Multi-Point Sense Amplifier and High-Speed Bit-Line Scheme for Embedded SRAM
II-Kwon Chang,Kae-Dal Kwack 한국정보과학회 1998 Journal of Electrical Engineering and Information Vol.3 No.3
This paper describes new sense amplifier with fast sensing delay time of 0.54ns and 32kb CMOS embedded SRAM with 4.67ns access time for a 3-V power supply. It was achieved using the sense amplifier with multiple point sensing scheme and high speed bit-line scheme. The sense amplifier saves 25% of the power dissipation compared with the conventional one while maintaining a very short sensing delay. The SRAM uses 0.5m double-polysilicon and triple-metal CMOS process technology. A die size is 1.78㎜×2.13㎜.
( Ii Seul Kwon ),( Joung Han Yim ),( Hong Kum Lee ),( Suhkneung Pyo ) 한국응용약물학회 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1
Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-α)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-α was significantly suppressed by the pre-treatment of lobaric acid (0.1-10 μg/ml) for 2 h. Lobaric acid abrogated TNF-α-induced NF-κB activity through preventing the degradation of IκB and phosphorylation of extracellular signalregulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-α receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-κB signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.
Kwon, Ii-Seul,Yim, Joung-Han,Lee, Hong-Kum,Pyo, Suhkneung The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.1
Lichens have been known to possess multiple biological activities, including anti-proliferative and anti-inflammatory activities. Vascular cell adhesion molecule-1 (VCAM-1) may play a role in the development of atherosclerosis. Hence, VCAM-1 is a possible therapeutic target in the treatment of the inflammatory disease. However, the effect of lobaric acid on VCAM-1 has not yet been investigated and characterized. For this study, we examined the effect of lobaric acid on the inhibition of VCAM-1 in tumor necrosis factor-alpha (TNF-${\alpha}$)-stimulated mouse vascular smooth muscle cells. Western blot and ELISA showed that the increased expression of VCAM-1 by TNF-${\alpha}$ was significantly suppressed by the pre-treatment of lobaric acid ($0.1-10{\mu}g/ml$) for 2 h. Lobaric acid abrogated TNF-${\alpha}$-induced NF-${\kappa}B$ activity through preventing the degradation of $I{\kappa}B$ and phosphorylation of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), and p38 mitogen activated protein (MAP) kinase. Lobaric acid also inhibited the expression of TNF-${\alpha}$ receptor 1 (TNF-R1). Overall, our results suggest that lobaric acid inhibited VCAM-1 expression through the inhibition of p38, ERK, JNK and NF-${\kappa}B$ signaling pathways, and downregulation of TNF-R1 expression. Therefore, it is implicated that lobaric acid may suppress inflammation by altering the physiology of the atherosclerotic lesion.