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Mutational analysis of TTK gene in gastric and colorectal cancers with microsatellite instability.
Ahn, Chang Hyeok,Kim, Yoo Ri,Kim, Sung Soo,Yoo, Nam Jin,Lee, Sug Hyung The Korean Cancer Association 2009 Cancer Research and Treatment Vol.41 No.4
<P>The TTK gene plays a crucial role in regulation of the mitotic checkpoint. The TTK gene has an A9 mononucleotide repeat in the coding sequences, which harbors mutations in gastric (GC) and colorectal cancers (CRC) with microsatellite instability (MSI). However, there are three more repeats (the A7s) in the coding sequences that have not been analyzed. The aim of this study was to explore whether the three A7s as well as the A9 are altered in GC and CRC, and to find any association of TTK mutation with clinocopathologic characteristics of GC and CRC.</P>
Chang, Seo‐,Yoon,Kim, Dong‐,Bin,Ryu, Gyeong Ryul,Ko, Seung‐,Hyun,Jeong, In‐,Kyung,Ahn, Yu‐,Bae,Jo, Yang‐,Hyeok,Kim, Myung‐,Jun Wiley Subscription Services, Inc., A Wiley Company 2013 Journal of cellular biochemistry Vol.114 No.4
<P><B>Abstract</B></P><P>Glucagon‐like peptide‐1 (GLP‐1) and its potent agonists have been widely studied in pancreatic islet β‐cells. However, GLP‐1 receptors are present in many extrapancreatic tissues including macrophages, and thus GLP‐1 may have diverse actions in these tissues and cells. Therefore, we examined the mechanism by which exendin‐4 (EX‐4), a potent GLP‐1 receptor agonist, inhibits lipopolysaccharide (LPS)‐induced iNOS expression in Raw264.7 macrophage cells. EX‐4 significantly inhibited LPS‐induced iNOS protein expression and nitrite production. However, Northern blot and promoter analyses demonstrated that EX‐4 did not inhibit LPS‐induced iNOS mRNA expression and iNOS promoter activity. Electrophoretic mobility shift assay (EMSA) showed that EX‐4 did not alter the binding activity of NF‐κB to the iNOS promoter. Consistent with the result of EMSA, LPS‐induced IκBα phosphorylation and nuclear translocation of p65 were not inhibited by EX‐4. Also, actinomycin D chase study and the promoter assay using the construct containing 3′‐untranslated region of iNOS showed that EX‐4 did not affect iNOS mRNA stability. Meanwhile, cycloheximide chase study demonstrated that EX‐4 significantly accelerated iNOS protein degradation. The EX‐4 inhibition of LPS‐induced iNOS protein was significantly reversed by adenylate cyclase inhibitors (MDL‐12330A and SQ 22536), a PKA inhibitor (H‐89) and PKAα gene silencing. These findings suggest that EX‐4 inhibited LPS‐induced iNOS expression at protein level, but not at transcriptional mechanism of iNOS gene and this inhibitory effect of EX‐4 was mainly dependent on cAMP/PKA system. J. Cell. Biochem. 114: 844–853, 2013. © 2012 Wiley Periodicals, Inc.</P>
급성 심근 경색 환자에서 재관류 방법에 따른 P파폭과 P파 분산의 변화
최웅길 ( Woong Gil Choi ),김대혁 ( Dae Hyeok Kim ),김기창 ( Gi Chang Kim ),안인선 ( In Sun Ahn ),김수현 ( Soo Hyun Kim ),유형권 ( Hyung Kwon Yu ),권준 ( Jun Kwan ),박금수 ( Keum Soo Park ),이우형 ( Woo Hyung Lee ) 대한내과학회 2007 대한내과학회지 Vol.73 No.5
목적: 급성 심근경색증 환자에서 심방세동은 10~20%의 빈도로 발생되는 흔한 부정맥이다. 최대 P파 폭과 P파 분산은 심방세동의 전기생리학적 특성과 연관된 동성 흥분파의 비균질 전도, 심방내 전도장애와 밀접히 연관된 것으로 알려져 있다. 이 연구의 목적은 급성 심근경색증 환자의 재관류 치료 방법이 최대 P파의 폭과 P파 분산에 대해 미치는 효과를 비교 분석하였다. 방법: 2005년 5월부터 2006년 5월까지 급성 심근경색으로 본원에 내원한 86명의 환자를 대상으로 응급실내원 당시의 모든 환자의 심전도와 일차적 관상동맥 중재술, 혈전용해요법을 시행 받은 환자 군은 치료 2일 후에 지연 관상동맥 중재술로 예정된 환자는 입원 2일 후의 심전도에서 최대 P파 폭과 P파 분산을 측정하여 각 군 간의 차이를 분석하였다. 결과: 일차적 관상동맥 중재술, 혈전용해요법, 지연관상동맥 중재술을 시행한 환자는 각각 28명, 27명 그리고 31명이었다. 일차적 관상동맥 중재술을 시행한 군이 다른 치료전략을 시행한 군에 비해 시술 후 최대 P파 폭과 P파 간격 분산이 다른 군에 비해 유의하게 감소하였으나, 혈전용해요법과 지연 관상동맥 중재술간의 치료후 유의한 차이는 없었다. 혈전용해요법과 지연 관상동맥 중재술을 시행한 경우 경색관련 관상동맥의 개존성이 있었던 군에서 개존성이 없었던 군에 비해 2일 후 P파 분산이 의미있게 감소하였다. 결론: 급성 심근경색증 환자에서 일차적 관상동맥중재술 군이 치료 후 최대 P파 폭과 P파 분산이 의미있게 감소하였다. Background: P wave dispersion (PWD) and P wave duration have been used to evaluate the discontinuous propagation of sinus impulse and the prolongation of atrial conduction time, respectively. This study was conducted to compare the change of the maximal P wave duration (Pmax) and PWD according to the treatment strategy used in patients with an acute myocardial infarction (AMI). Methods: We retrospectively evaluated 86 patients that experienced an AMI. Patients were classified into three groups according to the treatment strategy: primary percutaneous coronary intervention (PCI), thrombolytic therapy, and delayed PCI. ECGs that were obtained from all patients on admission and on the second day were analyzed. The Pmax and minimum P wave duration (Pmin) were measured from a 12-lead ECG. The PWD was calculated as the difference between the Pmax and Pmin. Result: There was no significant difference in the age, gender, medication, coronary risk factor, ejection fraction, left atrial diameter, basal Pmax and PWD among the groups. However, there were significant differences in P max and PWD between the primary PCI group and the other groups on the second day after hospital admission. In the thrombolytic therapy and delayed PCI groups, the PWD was significantly lower in the patients with a patent infarct-related artery (IRA) than in patients without a patent IRA on the second day after hospital admission. Conclusions: These findings suggest that a primary PCI decreased the Pmax and PWD more than thrombolytic therapy or a delayed PCI.(Korean J Med 73:489-495, 2007)