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Escherichia coli 패혈증 환자에 합병된 대칭적 하지 말단 괴사증 1예
남해성,유진홍,권순석,민준기,조현선,박민경,심병주,남유정,이지인,김진수,길욱현,조근종,신완식 대한감염학회 2005 감염과 화학요법 Vol.37 No.6
We have encountered a rare case of symmetrical peripheral gangrene complicating Escherichia coli sepsis in a 47-years-old male. He was successfully treated with antibiotics, anticoagulants, and vasodilator. To our knowledge, this is the first report on symmetrical peripheral gangrene complicating E. coli sepsis in Korea.
이수태,기해진,정순택,박양균 木浦大學校 工業技術硏究所 2000 工業技術硏究誌 Vol.10 No.-
Frozen dough of two flour, Tazo and Tazo-S, and two thawing, room and cold temperature, were determined to qualified bread quality. For best bread quality from frozen doughs, very strong flour should be used. Frozen doughs are increasingly being produced in the baking industry even though they generally provide bread with lower loaf volume than dose unfrozen fresh dough. Several investigators have reported that the major changes in doughs that have been frozen are related to yeast. During the dough fermentation, yeast produces carbon dioxide and flavor compounds. Loaf volume decreased markedly with freezing and thawing, and gradually during frozen storage.
요골 두 아탈구와 동반된 상완골 내 상과 골절 : 1예 보고 A Case Report
이한용,유기원,정진영,송주현,고해석,강용구,손문익 대한골절학회 2003 대한골절학회지 Vol.16 No.2
주관절 손산 중 상완골 내 상과 골절은 단독으로 혹은 주관절 탈구와 동반되어 발생하는 것이 일반적이다. 저자들은 15세 남자 환자의 좌측 요골 두 아탈구가 동반된 상완골 내 상과 골절을 경험하였다. 도수 정복을 시도하였으나 요골 두 아탈구의 정복을 얻을 수 없어 관혈적 정복술로 치료하엿다. 6개월추시 결과 후휴증이 없는 정상적인 관절 상태를 확인할 수 있었다. 연령, 원인 , 손상 기전으로 분석해 보면 이 동반 손상은 발생하기 매우 어렵고, 문헌 탐색 결과 현재까지 동일한 증례를 찾아볼 수 없었으므로 보고하는 바이다. It has been known that fracture of medial epicondylar apophysis of distal humerus may be isolated of associated with elbow deslocations. We have experienced a case which medial epicondylar fracture of the distal humerus was associated with subluxation of the radial head. Initially, we had tried reduction of subluxated radial head by closed method, but failed. Finally open reduction gad been performed. At 6 month after open reduction, clinical and radiological result were excellent. As it is difficult for those associated injuries to occur simultaneously and the similar cases never have been reported yet, we would like to present this case with a review of the literature.
Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy
Kee, Hae Jin,Kook, Hyun Hindawi Publishing Corporation 2011 Journal of biomedicine & biotechnology Vol.2011 No.-
<P>Cardiac hypertrophy occurs in association with heart diseases and ultimately results in cardiac dysfunction and heart failure. Histone deacetylases (HDACs) are post-translational modifying enzymes that can deacetylate histones and non-histone proteins. Research with HDAC inhibitors has provided evidence that the class I HDACs are pro-hypertrophic. Among the class I HDACs, HDAC2 is activated by hypertrophic stresses in association with the induction of heat shock protein 70. Activated HDAC2 triggers hypertrophy by inhibiting the signal cascades of either Krüppel like factor 4 (KLF4) or inositol polyphosphate-5-phosphatase f (Inpp5f). Thus, modulators of HDAC2 enzymes, such as selective HDAC inhibitors, are considered to be an important target for heart diseases, especially for preventing cardiac hypertrophy. In contrast, class IIa HDACs have been shown to repress cardiac hypertrophy by inhibiting cardiac-specific transcription factors such as myocyte enhancer factor 2 (MEF2), GATA4, and NFAT in the heart. Studies of class IIa HDACs have shown that the underlying mechanism is regulated by nucleo-cytoplasm shuttling in response to a variety of stress signals. In this review, we focus on the class I and IIa HDACs that play critical roles in mediating cardiac hypertrophy and discuss the non-histone targets of HDACs in heart disease. </P>
Kee, Hae Jin,Kim, Gwi Ran,Cho, Soo-Na,Kwon, Jin-Sook,Ahn, Youngkeun,Kook, Hyun,Jeong, Myung Ho The Korean Society of Cardiology 2014 Korean Circulation Journal Vol.44 No.4
<P><B>Background and Objectives</B></P><P>Differentiation and de-differentiation of vascular smooth muscle cells (VSMCs) are important events in atherosclerosis and restenosis after angioplasty. MicroRNAs are considered a key regulator in cellular processes such as differentiation, proliferation, and apoptosis. Here, we report the role of new miR-18a-5p microRNA and its downstream target genes in VSMCs and in a carotid balloon injury model.</P><P><B>Materials and Methods</B></P><P>Expression of miR-18a-5p and its candidate genes was examined in VSMCs and in a carotid artery injury model by quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and microRNA microarray analysis. VSMC differentiation marker genes including smooth muscle (SM) α-actin and SM22α were determined by Western blot, qRT-PCR, and a SM22α promoter study. Gene overexpression or knockdown was performed in VSMCs.</P><P><B>Results</B></P><P>miR-18a-5p was upregulated in the rat carotid artery at the early time after balloon injury. Transfection of the miR-18a-5p mimic promoted the VSMC differentiation markers SM α-actin and SM22α. In addition, miR-18a-5p expression was induced in differentiated VSMCs, whereas it decreased in de-differentiated VSMCs. We identified syndecan4 as a downstream target of miR-18-5p in VSMCs. Overexpression of syndecan4 decreased Smad2 expression, whereas knockdown of syndecan4 increased Smad2 expression in VSMCs. Finally, we showed that Smad2 induced the expression of VSMC differentiation marker genes in VSMCs.</P><P><B>Conclusion</B></P><P>These results indicate that miR-18a-5p is involved in VSMC differentiation by targeting syndecan4.</P>
Kee, Hae Jin,Sohn, Il Suk,Nam, Kwang Il,Park, Jong Eun,Qian, Yong Ri,Yin, Zhan,Ahn, Youngkeun,Jeong, Myung Ho,Bang, Yung-Jue,Kim, Nacksung,Kim, Jong-Keun,Kim, Kyung Keun,Epstein, Jonathan A.,Kook, Hyu American Heart Association 2006 Circulation Vol.113 No.1
<P>BACKGROUND: A number of distinct stress signaling pathways in myocardium cause cardiac hypertrophy and heart failure. Class II histone deacetylases (HDACs) antagonize several stress-induced pathways and hypertrophy. However, cardiac hypertrophy induced by transgenic overexpression of the homeodomain only protein, HOP, can be prevented by the nonspecific HDAC inhibitors trichostatin A and valproic acid, suggesting that alternate targets that oppose class II HDAC function might exist in myocardium. We tested the effects of several HDAC inhibitors, including a class I HDAC-selective inhibitor, SK-7041, on cardiac hypertrophy induced by angiotensin II (Ang II) treatment or aortic banding (AB). METHODS AND RESULTS: Cardiac hypertrophy was induced by chronic infusion of Ang II or by AB in mice or rats and evaluated by determining the ratio of heart weight to body weight or to tibia length, cross-sectional area, or echocardiogram. Cardiac hypertrophy induced by Ang II or AB for 2 weeks was significantly reduced by simultaneous administration of trichostatin A, valproic acid, or SK-7041. Echocardiogram revealed that exaggerated left ventricular systolic dimensions were relieved by HDAC inhibitors. HDAC inhibitors partially reversed preestablished cardiac hypertrophy and improved survival of AB mice. The expressions of atrial natriuretic factor, alpha-tubulin, beta-myosin heavy chain, and interstitial fibrosis were reduced by HDAC inhibition. CONCLUSIONS: These results suggest that the predominant effect of HDAC inhibition, mainly mediated by class I HDACs, is to prevent cardiac hypertrophy in response to a broad range of agonist and stretch stimuli.</P>