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Triamcinolone Acetonide에 의한 口蓋裂 발생기전에 관한 조직화학적 관찰
催奎南,全容赫,羅福瑛 고려대학교 의과대학 1986 고려대 의대 잡지 Vol.23 No.1
Physiologic levels of corticosteroids along with other hormones and growth factors are known to be essential for normal development of the secondary palate whereas, pharmacologic dose of these steroids specifically disrupt palatal development but still mechanism of their teratogenic action remains controversial and little have been reported on their effect on cell surface materials. Therefore, changes of palatal matrix components and carbohydrate rich cell surface macromolecules during the process of triamcinolone-induced cleft palate in DDY mouse in vivo mere investigated histochemically. Administration of triamcinolone acetonide delayed palatal shelf elevation and changed the shape of shelves to thicker and shorter, when the shelves finally reached horizontally, the distance between shelves was too far to contact each other but under these circumstances, no difference was seen in the palatal tissue histologically including medial edge epithelial degenerative change. PAS positive reactivity was great!:; increased in the shelf epithelia just prior to elevation and diastase sensitive materials were increased both in mesenchyme and epithelia prior to and during fusion and decreased thereafter. Whereas, TAC markedly reduced its reactivity prior to shelf elevation but the reactivity on diastase resistant PAS materials were recovered thereafter which suggest that the fluctuation of PAS positive materials largely depend on morphogenetic status of the palatal shelves. Sulfated acid mucopolysaccharide was increased in mesenchyme trnasiently prior to shelf elevation but T.4C inhibited its increment. With the results, it seems that TAC-induced cleft palate is primarily due to changes in quantity and quality of the palatal matrix and cell surface macromolecules with consequent morphological change of palatal shelves and interference of morphogenetic movement, shelf elevation.
박준수,송성진,김영환,조현,임수용,윤남균,이정기,박영주 한국비파괴검사학회 2003 학술대회 논문집 Vol.- No.1
Ultrasonic testing method has been developed to evaluate adhesive layers in blast tube for the reliability of the rocket. The main objective of the present work was to find debonding and uncharged state between steel and FRP layers. We distinguish the debonding and uncharged state using the resonance method in the adhesive layers. It was found that the higher magnitude of ultrasound is reflected for the uncharged area in frequency domain, and shown good agreements with experimental results. The traditional ultrasonic pulse-echo method offers good implements for the distinction debonding area. The nondestructive testing results were compared with the micrography of destruective testing. As results, ultrasonic testing could be utilized for the evaluation of adhesive layer in the blast tube.
Small Heterodimer Partner Blocks Cardiac Hypertrophy by Interfering With GATA6 Signaling
Nam, Yoon Seok,Kim, Yoojung,Joung, Hosouk,Kwon, Duk-Hwa,Choe, Nakwon,Min, Hyun-Ki,Kim, Yong Sook,Kim, Hyung-Seok,Kim, Don-Kyu,Cho, Young Kuk,Kim, Yong-Hoon,Nam, Kwang-Il,Choi, Hyoung Chul,Park, Dong H American Heart Association, Inc. 2014 Circulation research Vol.115 No.5
<P><B><U>Rationale</U>:</B></P><P>Small heterodimer partner (SHP; NR0B2) is an atypical orphan nuclear receptor that lacks a conventional DNA-binding domain. Through interactions with other transcription factors, SHP regulates diverse biological events, including glucose metabolism in liver. However, the role of SHP in adult heart diseases has not yet been demonstrated.</P><P><B><U>Objective</U>:</B></P><P>We aimed to investigate the role of SHP in adult heart in association with cardiac hypertrophy.</P><P><B><U>Methods and Results</U>:</B></P><P>The roles of SHP in cardiac hypertrophy were tested in primary cultured cardiomyocytes and in animal models. SHP-null mice showed a hypertrophic phenotype. Hypertrophic stresses repressed the expression of SHP, whereas forced expression of SHP blocked the development of hypertrophy in cardiomyocytes. SHP reduced the protein amount of Gata6 and, by direct physical interaction with Gata6, interfered with the binding of Gata6 to GATA-binding elements in the promoter regions of natriuretic peptide precursor type A. Metformin, an antidiabetic agent, induced SHP and suppressed cardiac hypertrophy. The metformin-induced antihypertrophic effect was attenuated either by SHP small interfering RNA in cardiomyocytes or in SHP-null mice.</P><P><B><U>Conclusions</U>:</B></P><P>These results establish SHP as a novel antihypertrophic regulator that acts by interfering with GATA6 signaling. SHP may participate in the metformin-induced antihypertrophic response.</P>
U. Yong(용의중),D. Kim(김동환),H. Kim(김호중),D. G. Hwang(황동규),S. Cho(조성건),H. Nam(남효영),S. Kim(김세진),T. Y. Kim(김태영),U. Jeong(정운룡),K. Kim(김기훈),W. K. Chung(정완균),W. H. Yeo(여운홍),J. Jang(장진아) Korean Society for Precision Engineering 2021 한국정밀공학회 학술발표대회 논문집 Vol.2021 No.11월
Over the years, engineered heart tissue (EHT), composed of cardiac cells and a hydrogel, has been considered as a promising in-vitro cardiac model in that it can reproduce the physiological contractions of an actual animal heart. In particular, the contractile force of EHT is one of the representative factors to evaluate drug-induced cardiotoxicity that is a major cause of the withdrawal of drug development. Although there have been a lot of methods to monitor the contractile force of the EHT, most of them are based on optical readout systems that have to process a huge amount of image data. Recently, a strain gauge-based microphysiological system was developed to monitor the contractile force of a laminar cardiac tissue, which can acquire real-time data with a relatively small amount of data. However, the system can monitor only few layers of cardiomyocytes, which are physiologically less relevant environment compared to EHT. Here, we developed a hybrid bioprinted tissue platform, consisting of six bipillar-grafted strain gauges (BPSGs) and one wireless device, that enables online monitoring of the contractile forces from 6 different EHTs in real time during culturing. Furthermore, we confirmed that our system can detect the effects of commercially available drugs on EHTs.
Yong-Hee Kim,Thakor, Nitish V.,Schieber, Marc H.,Hyoung-Nam Kim IEEE 2015 IEEE transactions on neural systems and rehabilita Vol.23 No.3
<P>Future generations of brain-machine interface (BMI) will require more dexterous motion control such as hand and finger movements. Since a population of neurons in the primary motor cortex (M1) area is correlated with finger movements, neural activities recorded in M1 area are used to reconstruct an intended finger movement. In a BMI system, decoding discrete finger movements from a large number of input neurons does not guarantee a higher decoding accuracy in spite of the increase in computational burden. Hence, we hypothesize that selecting neurons important for coding dexterous flexion/extension of finger movements would improve the BMI performance. In this paper, two metrics are presented to quantitatively measure the importance of each neuron based on Bayes risk minimization and deflection coefficient maximization in a statistical decision problem. Since motor cortical neurons are active with movements of several different fingers, the proposed method is more suitable for a discrete decoding of flexion-extension finger movements than the previous methods for decoding reaching movements. In particular, the proposed metrics yielded high decoding accuracies across all subjects and also in the case of including six combined two-finger movements. While our data acquisition and analysis was done off-line and post processing, our results point to the significance of highly coding neurons in improving BMI performance.</P>