• 제목/요약/키워드: CYP2C9

검색결과 94건 처리시간 0.023초

인후두위산역류증(Laryngopharyngeal Reflux: LPR)의 치료에 대한 RabeprazoleSodium(Parietd)의 임상효과와 안전성 검토 (Clinical Study for Efficacy and Safety of Rabeprazole Sodium(Pariet) in the Treatment of Laryngopharyngeal Reflex(LPR) Disease)

  • 정광윤;전병선;고상현;권기환;권순영;권중근;김동영;김상철;김성완;김영모;김영호;김윤환;김장묵
    • 대한기관식도과학회지
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    • 제10권2호
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    • pp.35-42
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    • 2004
  • Background and objective : Rabeprazole is a new generation proton pump inhibitor, which has a rapid onset after first dose, predictable efficacy in all patients regardless of CYP2C19 genotype status, and less nocturnal acid breakthrough. The aim of the study is to investigate clinical efficacy and safety of rabeprazole sodium (Pariet 10mg qd)when administered once daily to patients with laryngopharyngeal reflux(LPR) disease. Methods : Among the patients who had visited the Department of Otolaryngology, those with LPR symptoms, had undergone laryngoscopy. Symptoms and endoscopic laryngeal sings were recorded initially, at 1 month, 2 months, 3 months, and more than 3 months, All patients were evaluated for clinical efficacy on the basis of symptom scores, reflux finding score(RFS), and side effects. Results : In general, most symptom scores and RFS improved over the time. Efficacy of the Pariet on LPR-related symptoms were $63.2\%,\;77.5\%,\;78.7\%,\;and\;90.9\%$ before 4 weeks, 4 to 8 weeks, 8 to 12 weeks, and after 12 weeks respectively. Efficacy on the RFS were $61.8\%,\;78.4\%,\;82.9\%,\;and\;85.5\%$ before 4 weeks, 4 to 8 weeks, 8 to 12 weeks, and after 12 weeks respectively. Pariet was well tolerated and was associated with few drug-related side effects. Conclusion Because of its efficacy and safety, Pariet may prove to be an alternative to currently available proton pump inhibitors.

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Finding Genes Discriminating Smokers from Non-smokers by Applying a Growing Self-organizing Clustering Method to Large Airway Epithelium Cell Microarray Data

  • Shahdoust, Maryam;Hajizadeh, Ebrahim;Mozdarani, Hossein;Chehrei, Ali
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권1호
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    • pp.111-116
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    • 2013
  • Background: Cigarette smoking is the major risk factor for development of lung cancer. Identification of effects of tobacco on airway gene expression may provide insight into the causes. This research aimed to compare gene expression of large airway epithelium cells in normal smokers (n=13) and non-smokers (n=9) in order to find genes which discriminate the two groups and assess cigarette smoking effects on large airway epithelium cells.Materials and Methods: Genes discriminating smokers from non-smokers were identified by applying a neural network clustering method, growing self-organizing maps (GSOM), to microarray data according to class discrimination scores. An index was computed based on differentiation between each mean of gene expression in the two groups. This clustering approach provided the possibility of comparing thousands of genes simultaneously. Results: The applied approach compared the mean of 7,129 genes in smokers and non-smokers simultaneously and classified the genes of large airway epithelium cells which had differently expressed in smokers comparing with non-smokers. Seven genes were identified which had the highest different expression in smokers compared with the non-smokers group: NQO1, H19, ALDH3A1, AKR1C1, ABHD2, GPX2 and ADH7. Most (NQO1, ALDH3A1, AKR1C1, H19 and GPX2) are known to be clinically notable in lung cancer studies. Furthermore, statistical discriminate analysis showed that these genes could classify samples in smokers and non-smokers correctly with 100% accuracy. With the performed GSOM map, other nodes with high average discriminate scores included genes with alterations strongly related to the lung cancer such as AKR1C3, CYP1B1, UCHL1 and AKR1B10. Conclusions: This clustering by comparing expression of thousands of genes at the same time revealed alteration in normal smokers. Most of the identified genes were strongly relevant to lung cancer in the existing literature. The genes may be utilized to identify smokers with increased risk for lung cancer. A large sample study is now recommended to determine relations between the genes ABHD2 and ADH7 and smoking.

Effects of Pahs and Pcbs and Their Toxic Metabolites on Inhibition of Gjic and Cell Proliferation in Rat Liver Epithelial Wb-F344 Cells

  • Miroslav, Machala;Jan, Vondracek;Katerina, Chramostova;Lenka, Sindlerova;Pavel, Krcmar;Martina, Pliskova;Katerina, Pencikova;Brad, Upham
    • 한국환경성돌연변이발암원학회지
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    • 제23권2호
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    • pp.56-62
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    • 2003
  • The liver progenitor cells could form a potential target cell population fore both tumor-initiating and -promoting chemicals. Induction of drug-metabolizing and antioxidant enzymes, including AhR-dependent CYP1A1, NQO-1 and AKR1C9, was detected in the rat liver epithelial WB-F344 "stem-like" cells. Additionally, WB-F344 cells express a functional, wild-type form of p53 protein, a biomarker of genotoxic events, and connexin 43, a basic structural unit of gap junctions forming an important type of intercellular communication. In this cellular model, two complementary assays have been established for detection of the modes of action associated with tumor promotion: inhibition of gap junctional intercellular communication (GJIC) and proliferative activity in confluent cells. We found that the PAHs and PCBs, which are AhR agonists, released WB-F344 cells from contact inhibition, increasing both DNA synthesis and cell numbers. Genotoxic effects of some PAHs that lead to apoptosis and cell cycle delay might interfere with the proliferative activity of PAHs. Contrary to that, the nongenotoxic low-molecular-weight PAHs and non-dioxin-like PCB congeners, abundant in the environment, did not significantly affect cell cycle and cell proliferation; however both groups of compounds inhibited GJIC in WB-F344 cells. The release from contact inhibiton by a mechanism that possibly involves the AhR activation, inhibition of GJIC and genotoxic events induced by environmental contaminants are three important modes of action that could play an important role in carcinogenic effects of toxic compounds. The relative potencies to inhibit GJIC, to induce AhR-mediated activity, and to release cells from contact inhibition were determined for a large series of PAHs and PCBs and their metabolites. In vitro bioassays based on detection of events on cellular level (deregulation of GJIC and/or proliferation) or determination of receptor-mediated activities in both ?$stem-like^{\circ}{\times}$ and hepatocyte-like liver cellular models are valuable tools for detection of modes of action of polyaromatic hydrocarbons. They may serve, together with concentration data, as a first step in their risk assessment.

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제조방법에 따른 떫은감 (Diosyros kaki Thumb.)의 대사체 프로파일링과 중성지질/콜레스테롤 대사 관련 유전자발현 연구 : in vitro 및 in vivo 연구 (Metabolites profiling and hypolipidemic/hypocholesterolemic effects of persimmon (Diosyros kaki Thumb.) by different processing procedures: in vitro and in vivo studies)

  • 박수연;오은경;임예니;신지윤;정희아;박송이;이진희;최정숙;권오란
    • Journal of Nutrition and Health
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    • 제51권4호
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    • pp.275-286
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    • 2018
  • 본 연구는 떫은감 청도반시의 분말을 열수 추출하고 칼럼 추출하는 과정에서 획득한 PWE와 TEP에 대한 대사체 프로파일을 분석하고, 유리지방산을 처리한 HepG2 세포와 식이로 고지혈증을 유도한 Wistar계 흰쥐의 간조직을 사용하여 중성지질 및 콜레스테롤 대사 관련 유전자 발현을 측정하였다. 대사체 분석은 가스크로마토그래프-질량분석법과 액체크로마토그래프-질량분석법을 사용하였으며, PLS-DA 분석과 heatmap 분석을 실시한 결과 PWE는 떫은감 분말과 비교적 유사한 대사체 프로파일을, 그리고 TEP는 떫은감 분말과 매우 다른 대사체 프로파일을 가지고 있음을 확인하였다. 세포실험과 또한 세포실험에서 얻어진 결과를 검증하기 위해 수행된 동물실험에서 PWE와 TEP는 모두 SREBP1c와 FAS 유전자 발현을 감소하여 간의 지방축적을 감소시키는 것으로 관찰되었으나, 콜레스테롤 축적을 억제하는 효능은 PWE에 비해 TEP에서 우세하게 증가하는 것이 관찰되었다. 특별히 TEP는 SREBP2, HMGCR 유전자 발현을 억제하고 LDLR 유전자 발현을 촉진하는 것으로 나타났다. TEP는 탄닌 중 Gallic acid 그리고 장쇄지방산아미드인 Oleamide와 Palmitamide 함량이 유의하게 증가되었으므로, 향후 이들 성분과 타깃 유전자의 상관성을 분석하고, 이를 통해 시스템네트워크로 나타내어 대사체 프로파일에 따른 지질 및 콜레스테롤 대사 간 상호 영향을 추가적으로 연구해야 할 것으로 사료된다.